subject:(Insulin receptor)

University of Canterbury

1. Subramanian, Kannan. Kinetics of insulin - insulin receptor interaction using a surface plasmon resonance (SPR).

Degree: PhD, Chemical Engineering, 2014, University of Canterbury

URL: http://dx.doi.org/10.26021/2927

► Type 2 diabetes or adult onset diabetes, has been a global epidemic for the past two decades, and the number of new cases accelerates every… (more)

▼ Type 2 diabetes or adult onset diabetes, has been a global epidemic for the past two decades, and the number of new cases accelerates every year. Insulin resistance is one of the major factors behind this, wherein the insulin receptor, which signals to regulate glucose levels, based on the hormone insulin, loses its sensitivity. Obesity is one other major concern which is caused due to the improper balance between the caloric intake and the energy utilized. Gastric bypass surgeries (GBP) are performed to avert obesity. However, a beneficial side-effect is that the state of insulin resistance is reset to near baseline levels within a few days after the procedure. The reason behind this remains unexplained, with possible humoral effects, hypothesized to occur after the bariatric procedure. In this work, high-five insect cell line was utilized to recombinantly produce full length insulin receptors (IR). However commercially sourced IR ectodomains (eIR – soluble version of the full length IR with the completely extracellular α subunits along with extracellular and transmembrane regions of the β subunit), were used to study the interaction. Measuring the kinetics of IR-insulin interactions is critical to improving our understanding of this disease. In this study, a multiplex surface plasmon resonance (SPR) assay was developed for studying the interaction between insulin and the eIR. A scaffold approach was used in which anti-insulin receptor monoclonal antibody 83–7 (Abcam, Cambridge, UK) was first immobilized on the SPR sensorchip by amine coupling, followed by eIR capture. The multiplex SPR system (ProteOn XPR36TM, Bio-Rad Laboratories, Hercules, CA) enabled measurement of replicate interactions with a single, parallel set of analyte injections, whereas repeated regeneration of the scaffold between measurements caused variable loss of antibody activity. The main approach was to replicate the physiological IR-insulin interaction using this assay. It was also observed that insulin at higher concentrations tend to form dimers and hexamers in solution. This was tested using size exclusion chromatography analysis and proved to be true. Therefore an alternative analyte with the similar binding properties and affinity of insulin and at the same time with reduced self- association characteristics was explored. Lispro, the analogue of insulin with reduced self-association properties (generated by swapping of residue 28 and 29 with Lys and Pro respectively) was finally used to study the interaction with eIR. Interactions between recombinant human insulin with eIR-A (A isoform of the insulin receptor ectodomain) followed a two-site binding pattern (consistent with the literature), with a high-affinity site (dissociation constant KD1 = 38.1 ± 0.9 nM) and a low-affinity site (KD2 = 166.3 ± 7.3 nM). The predominantly monomeric insulin analogue Lispro had corresponding dissociation constants KD1 =73.2 ± 1.8 nM and KD2 =148.9 ± 6.1 nM, but the fit to kinetic data was improved when conformational change factor was included in which…

Subjects/Keywords: insulin; insulin-receptor; kinetics; surface plasmon resonance

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APA (6^th Edition):

Subramanian, K. (2014). Kinetics of insulin - insulin receptor interaction using a surface plasmon resonance (SPR). (Doctoral Dissertation). University of Canterbury. Retrieved from http://dx.doi.org/10.26021/2927

Chicago Manual of Style (16^th Edition):

Subramanian, Kannan. “Kinetics of insulin - insulin receptor interaction using a surface plasmon resonance (SPR).” 2014. Doctoral Dissertation, University of Canterbury. Accessed March 03, 2021. http://dx.doi.org/10.26021/2927.

MLA Handbook (7^th Edition):

Subramanian, Kannan. “Kinetics of insulin - insulin receptor interaction using a surface plasmon resonance (SPR).” 2014. Web. 03 Mar 2021.

Vancouver:

Subramanian K. Kinetics of insulin - insulin receptor interaction using a surface plasmon resonance (SPR). [Internet] [Doctoral dissertation]. University of Canterbury; 2014. [cited 2021 Mar 03]. Available from: http://dx.doi.org/10.26021/2927.

Council of Science Editors:

Subramanian K. Kinetics of insulin - insulin receptor interaction using a surface plasmon resonance (SPR). [Doctoral Dissertation]. University of Canterbury; 2014. Available from: http://dx.doi.org/10.26021/2927

University of Adelaide

2. Bonython, Eric Richard. Investigation of insulin-like receptor systems.

Degree: 2005, University of Adelaide

URL: http://hdl.handle.net/2440/59217

► The insulin and insulin-like growth factor receptor (IR and IGF-lR respectively) networks are ancient and fundamental systems that control growth and metabolism in multicellular organisms.… (more)

▼ The insulin and insulin-like growth factor receptor (IR and IGF-lR respectively) networks are ancient and fundamental systems that control growth and metabolism in multicellular organisms. This thesis has examined several aspects of this field focusing on mammalian receptor biology and a comparison of the similarities and differences between the insulin and IGF receptor signalling systems. The insulin receptor family of proteins consist of eleven structural domains, of which the extracellular domains contain all the ligand binding and specificity determinants. The insert domain, within the extracellular region is the least understood of all the domains, and it has no similarity to any other protein sequence. It does however contain the cleavage site which separates the receptor into two subunits and also a small stretch of residues shown to directly contact bound ligand and which is absolutely required for ligand binding in short recombinant forms of the receptor. In addition, the human insulin receptor, expressed as one of two isoforms, A and B, results in the exclusion or inclusion of 12 amino acids directly adjacent to the ligand contacting amino acids in the insert domain. The A isoform lacking exon11 is expressed ubiquitously and the B isoform containing exon11 is co-expressed mainly in the traditional insulin responsive tissues of liver, muscle, adipocytes and kidney, where it is the dominant isoform. In this thesis recombinant insert domain was expressed in a bacterial system in an attempt to purify folded protein suitable for NMR structural analysis. The results of the expression studies indicated that the insert domain was unstructured in isolation and was unable to be adequately refolded by all conditions tried, although hydrophobic conditions appeared to partially stabilize the structure. The overall conclusions of this project were that the Insert domain is likely to have limited structure, and probably buried within the receptor, and therefore requires the presence of the rest of the extracellular domains to adopt its correct structure. A comparison of the ligand binding and phsophorylation potential between the two human isoforms of the insulin receptor was made. A competition binding assay using europium labelled insulin was developed, that found that both IGF-l and IGF-2 had an increased affinity for the hIR-A, but insulin had a slightly reduced affinity. These results differ from the established literature in the raw values, however the relative ratios of binding strength are consistent. The most likely reason for this is that the europium labelled insulin has a different mode of binding the receptors due to the location of the europium chelate. Interestingly, using europium labelled IGF-l produced results nearly identical to those of conventional competition assays. Phosphorylation assays indicated that the hIR-B isoform was more responsive than hIR-A. Even though IGF-2 and IGF-l had improved affinity for hIR-A, the level of phosphorylation was not as high. The ability of each growth factor… Advisors/Committee Members: School of Molecular and Biomedical Science : Biochemistry (school).

Subjects/Keywords: insulin; receptor

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APA (6^th Edition):

Bonython, E. R. (2005). Investigation of insulin-like receptor systems. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/59217

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Bonython, Eric Richard. “Investigation of insulin-like receptor systems.” 2005. Thesis, University of Adelaide. Accessed March 03, 2021. http://hdl.handle.net/2440/59217.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Bonython, Eric Richard. “Investigation of insulin-like receptor systems.” 2005. Web. 03 Mar 2021.

Vancouver:

Bonython ER. Investigation of insulin-like receptor systems. [Internet] [Thesis]. University of Adelaide; 2005. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2440/59217.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Bonython ER. Investigation of insulin-like receptor systems. [Thesis]. University of Adelaide; 2005. Available from: http://hdl.handle.net/2440/59217

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Minnesota

3. Fagan, Dedra Hannah. Examination of molecular changes in acquired tamoxifen resistance and subsequent response to anti-IGF1R therapy.

Degree: PhD, 2012, University of Minnesota

URL: http://purl.umn.edu/131512

► The type-I insulin like growth factor (IGF1R) contributes to the proliferation, survival, and metastasis of breast cancer cells. Disruption of IGF1R signaling alone or in… (more)

▼ The type-I insulin like growth factor (IGF1R) contributes to the proliferation, survival, and metastasis of breast cancer cells. Disruption of IGF1R signaling alone or in combination with established therapies has emerged as an important strategy in cancer therapy. Several anti-IGF1R antibodies and tyrosine kinase inhibitors (TKI's) are being evaluated in phase I, II, or III clinical trials, often in endocrine resistant populations. Thus far, clinical trials have provided less than promising results. Although preclinical studies showed promising results, these studies were performed using endocrine sensitive cell models. Here, we sought to determine the efficacy of IGF1R inhibitors using an endocrine resistant human breast cancer cell model in vitro and in vivo. The first section of this work highlights the creation and characterization of a tamoxifen-resistant (TamR) cell line. We demonstrate in two estrogen receptor positive breast cancer cell lines that TamR cells maintain estrogen receptor expression. Levels of IGF1R, a known estrogen regulated gene, were greatly reduced in TamR cells. Further, signaling, proliferation, and anchorage-independent growth through the receptor were abolished in TamR cells. Interestingly, signaling and growth through the closely related insulin receptor (a non-estrogen regulated gene) remained intact in TamR cells. The second part of this work utilizes TamR cells to examine the efficacy of IGF1R inhibitors in endocrine resistant and sensitive breast cancer cells. We show that the signaling, proliferation, and anchorage-independent growth of endocrine sensitive MCF-7 cells can be inhibited using a variety of IGF1R antibodies. TamR cells, which lack IGF1R expression, are not affected by IGF1R antibody treatment in vitro or in vivo. In contrast, tyrosine kinase inhibitors which can inhibit both IGF1R and IR were able to inhibit the signaling, proliferation, and anchorage-independent growth of both TamR and parental cells. Taken together, our data demonstrate that tamoxifen resistant cells and tamoxifen treated xenografts have reduced levels of IGF1R, making IGF1R antibody treatment ineffective. Our work highlights the importance of evaluating new therapies using a preclinical model that matches the patient population the therapy will be used in. Finally, our data suggest that inhibition of IR may be necessary to manage tamoxifen resistant breast cancer.

Subjects/Keywords: Endocrine resistance; IGF1R; Insulin receptor; Pharmacology

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APA (6^th Edition):

Fagan, D. H. (2012). Examination of molecular changes in acquired tamoxifen resistance and subsequent response to anti-IGF1R therapy. (Doctoral Dissertation). University of Minnesota. Retrieved from http://purl.umn.edu/131512

Chicago Manual of Style (16^th Edition):

Fagan, Dedra Hannah. “Examination of molecular changes in acquired tamoxifen resistance and subsequent response to anti-IGF1R therapy.” 2012. Doctoral Dissertation, University of Minnesota. Accessed March 03, 2021. http://purl.umn.edu/131512.

MLA Handbook (7^th Edition):

Fagan, Dedra Hannah. “Examination of molecular changes in acquired tamoxifen resistance and subsequent response to anti-IGF1R therapy.” 2012. Web. 03 Mar 2021.

Vancouver:

Fagan DH. Examination of molecular changes in acquired tamoxifen resistance and subsequent response to anti-IGF1R therapy. [Internet] [Doctoral dissertation]. University of Minnesota; 2012. [cited 2021 Mar 03]. Available from: http://purl.umn.edu/131512.

Council of Science Editors:

Fagan DH. Examination of molecular changes in acquired tamoxifen resistance and subsequent response to anti-IGF1R therapy. [Doctoral Dissertation]. University of Minnesota; 2012. Available from: http://purl.umn.edu/131512

University of Iowa

4. Starks, Rachel Diaz. Molecular basis of insulin resistance in Bardet Biedl syndrome.

Degree: PhD, Molecular and Cell Biology, 2015, University of Iowa

URL: https://ir.uiowa.edu/etd/5641

► Bardet Biedl Syndrome (BBS) displays heterogeneity in the genes involved and clinical features. Mutations in 19 genes have been associated with BBS. Eight BBS… (more)

Subjects/Keywords: BBSome; BBS proteins; glucose homeostasis; insulin receptor; insulin resistance; Cell Biology

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APA (6^th Edition):

Starks, R. D. (2015). Molecular basis of insulin resistance in Bardet Biedl syndrome. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/5641

Chicago Manual of Style (16^th Edition):

Starks, Rachel Diaz. “Molecular basis of insulin resistance in Bardet Biedl syndrome.” 2015. Doctoral Dissertation, University of Iowa. Accessed March 03, 2021. https://ir.uiowa.edu/etd/5641.

MLA Handbook (7^th Edition):

Starks, Rachel Diaz. “Molecular basis of insulin resistance in Bardet Biedl syndrome.” 2015. Web. 03 Mar 2021.

Vancouver:

Starks RD. Molecular basis of insulin resistance in Bardet Biedl syndrome. [Internet] [Doctoral dissertation]. University of Iowa; 2015. [cited 2021 Mar 03]. Available from: https://ir.uiowa.edu/etd/5641.

Council of Science Editors:

Starks RD. Molecular basis of insulin resistance in Bardet Biedl syndrome. [Doctoral Dissertation]. University of Iowa; 2015. Available from: https://ir.uiowa.edu/etd/5641

Cleveland State University

5. Liu, Danting. RNASE L MEDIATES GLUCOSE HOMEOSTASIS THROUGH REGULATING THE INSULIN SIGNALING PATHWAY.

Degree: PhD, College of Sciences and Health Professions, 2018, Cleveland State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=csu1544627440336052

► Diabetes is characterized by hyperglycemia mainly due to defect in insulin secretion and/or action. Regulation of glucose transport and use by insulin is central to… (more)

▼ Diabetes is characterized by hyperglycemia mainly due to defect in insulin secretion and/or action. Regulation of glucose transport and use by insulin is central to the maintenance of whole-body glucose homeostasis. One of the potential mechanisms associated with insulin sensitivity is the activation of insulin receptor (IR) and subsequently transduces the signal through phosphorylation of insulin receptor substrate (IRS) and activation of the PI-3K/Akt pathway. In contrast, activation of the mammalian target of rapamycin (mTOR) and ribosomal protein S6 kinase (p70S6K) suppresses the signal cascade. RNase L, an interferon (IFN)-inducible enzyme, plays an important role in IFN functions against viral infection and cell proliferation. However, a direct link between RNase L and insulin sensitivity has yet to be clearly established. RNase L+/+ and -/- mouse embryonic fibroblasts (MEFs) and hepatocytes were used to investigate the role of RNase L in insulin signaling and sensitivity. Cells were treated with insulin at various time points and different concentrations. Activation of the insulin signaling pathway was determined by immunoblot analyses for the protein level and phosphorylation status of these components such as IR/p-IR, IRS1/p-IRS1 and AKT/p-AKT in the presence or absence of a chemical inhibitor. Interestingly, we found that RNase L might mediate insulin signaling and glucose homeostasis through impacting insulin receptor (IR) which is a trans-membrane receptor activated by insulin. The phosphorylation status of IR was significantly reduced in the cell deficient RNase L. As a result, activation of downstream components in the insulin signaling pathway and the PI3K/AKT pathway was significantly inhibited in RNase L-/- cells. Further investigation of the molecular mechanism underlying the role of RNase L in mediating the activation of IR revealed that RNase L might regulate cleaving the precursor of IR and activating IRS-1 via the ubiquitin/ proteasome system. Our results obtained from this study provide a better understanding of RNase L functions and open a new horizon for its role in the metabolic system besides in the defense of viral infection. Advisors/Committee Members: Zhou, Aimin (Committee Chair).

Subjects/Keywords: Biochemistry; Molecular Biology; RNASE L; Insulin Resistance; Insulin Receptor

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APA (6^th Edition):

Liu, D. (2018). RNASE L MEDIATES GLUCOSE HOMEOSTASIS THROUGH REGULATING THE INSULIN SIGNALING PATHWAY. (Doctoral Dissertation). Cleveland State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=csu1544627440336052

Chicago Manual of Style (16^th Edition):

Liu, Danting. “RNASE L MEDIATES GLUCOSE HOMEOSTASIS THROUGH REGULATING THE INSULIN SIGNALING PATHWAY.” 2018. Doctoral Dissertation, Cleveland State University. Accessed March 03, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=csu1544627440336052.

MLA Handbook (7^th Edition):

Liu, Danting. “RNASE L MEDIATES GLUCOSE HOMEOSTASIS THROUGH REGULATING THE INSULIN SIGNALING PATHWAY.” 2018. Web. 03 Mar 2021.

Vancouver:

Liu D. RNASE L MEDIATES GLUCOSE HOMEOSTASIS THROUGH REGULATING THE INSULIN SIGNALING PATHWAY. [Internet] [Doctoral dissertation]. Cleveland State University; 2018. [cited 2021 Mar 03]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=csu1544627440336052.

Council of Science Editors:

Liu D. RNASE L MEDIATES GLUCOSE HOMEOSTASIS THROUGH REGULATING THE INSULIN SIGNALING PATHWAY. [Doctoral Dissertation]. Cleveland State University; 2018. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=csu1544627440336052

University of Illinois – Urbana-Champaign

6. Cervantes, David. Modulation of mitogenic signaling and growth by sympathetic adrenergic regulation.

Degree: PhD, 0325, 2012, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/29837

► Heart disease and diabetes mellitus are growing epidemics, consistently ranking within the top ten causes of death in the United States. Both diseases are associated… (more)

▼ Heart disease and diabetes mellitus are growing epidemics, consistently ranking within the top ten causes of death in the United States. Both diseases are associated with cardiac remodeling, including cellular growth and fibrosis. Central to the progression of heart disease and diabetes are the adrenergic receptors (ARs) and insulin receptors (IR), respectively. Classically considered to elicit separate, and even opposing, cellular processes, increasing evidence suggests that ARs are capable of signaling cross-talk with other G-protein coupled receptors (GPCRs) as well as other receptor families, including receptor tyrosine kinases (RTKs). While the ARs have been implicated at numerous stages of heart failure, the adrenergic signaling mechanisms underlying this remodeling remain unknown. Further, studies investigating signaling cross-talk among different adrenergic receptors as well as between adrenergic receptors and other signaling pathways in myocardium remain in their infancy. In addition, few studies have implied functional interactions between IRs and βARs in cardiac tissues. Understanding how cells integrate information from a variety of chemically diverse signals into complex, orchestrated responses such as cell proliferation, differentiation and apoptosis is an overarching goal of cell biology. Thus, an understanding of the mechanisms and physiologic consequences of adrenergic receptor cross-talk within the heart is essential to develop novel treatments designed to prevent the cardiac remodeling observed in heart disease and diabetes. In concordance, the goals of this thesis research are two-fold. First, we aim to define mechanisms of AR cross-talk in cardiac cells. Secondly, we aim to determine the importance of these mechanisms in cardiac remodeling in response to pathological conditions. To begin to address the goals presented we first examined cross-talk within GPCRs. We elucidated a general mechanism in which non-traditional GPCR signaling is capable of regulating mitogen-activated protein kinase (MAPK) signaling originating from another GPCR. Interestingly, this cross-talk impaired GPCR-induced cellular proliferation. Next, we characterized a novel signaling mechanism in which type II RTK activation at high concentrations of mitogen can recruit non-traditional GPCR signaling components to fine-tune activation of MAPK signaling for cell proliferation. In sum, this work presents a significant expansion of our understanding of GPCR signaling cross-talk and its role in altering growth signaling originating from another receptor. Further, due to the complexities of hormonal signaling in vivo, this work highlights the need to further pursue a more in-depth understanding of how concomitant activation of one signaling pathway can alter the signaling and physiologic outcome of another receptor’s signaling. Advisors/Committee Members: Xiang, Yang (advisor), Nardulli, Ann M. (committee member), Chen, Jie (committee member), Raetzman, Lori T. (committee member).

Subjects/Keywords: adrenergic receptor; insulin receptor; extracellular signal-regulated kinase (ERK); heart; arrestin

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APA (6^th Edition):

Cervantes, D. (2012). Modulation of mitogenic signaling and growth by sympathetic adrenergic regulation. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/29837

Chicago Manual of Style (16^th Edition):

Cervantes, David. “Modulation of mitogenic signaling and growth by sympathetic adrenergic regulation.” 2012. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed March 03, 2021. http://hdl.handle.net/2142/29837.

MLA Handbook (7^th Edition):

Cervantes, David. “Modulation of mitogenic signaling and growth by sympathetic adrenergic regulation.” 2012. Web. 03 Mar 2021.

Vancouver:

Cervantes D. Modulation of mitogenic signaling and growth by sympathetic adrenergic regulation. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2142/29837.

Council of Science Editors:

Cervantes D. Modulation of mitogenic signaling and growth by sympathetic adrenergic regulation. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2012. Available from: http://hdl.handle.net/2142/29837

Texas A&M University

7. Lu, Hsiao Ling. Vitellogenin Receptor and Neuropeptide Receptors Involved in Reproduction of the Red Imported Fire Ant (Solenopsis invicta Buren).

Degree: PhD, Entomology, 2012, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2011-12-10218

► Social insects have complex forms of social organization. Molecular mechanisms involved in the regulation of their reproduction are not fully understood. This dissertation investigated the… (more)

▼ Social insects have complex forms of social organization. Molecular mechanisms involved in the regulation of their reproduction are not fully understood. This dissertation investigated the vitellogenin receptor (VgR), short neuropeptide F (sNPF) receptor, and two insulin receptors (InRs) in the red imported fire ant Solenopsis invicta, focusing on their possible roles in the regulation of queen reproduction. Knowledge of these receptors may provide novel ways to manipulate either reproductive castes or overall reproductive outcome, diminishing the fire ant impact as invasive pest. Fire ant virgin queens have more abundant VgR (SiVgR) transcripts than newly-mated queens, but limited egg formation. To elucidate whether queen maturation involved changes in SiVgR expression, we investigated both virgin and mated queens. In both queens, immunofluorescence analysis of ovaries revealed differential SiVgR localization in early and late stage oocytes; however, mated queens showed higher SiVgR expression than virgin queens. In virgin queens, the SiVgR signal was first observed at the oocyte membrane beginning at day 12 post-emergence, coinciding with the maturation period required before a mating flight. SiVgR silencing in virgins through RNA interference abolished egg formation, demonstrating that SiVgR is involved in queen ovarian development pre-mating. The sNPF and insulin signaling pathways have been implicated in the regulation of food intake and body size, and these peptides also play a gonadotropic role in the ovaries of some insect species. To elucidate the sites of action of the sNPF peptide(s), the sNPF receptor tissue expression and cellular localization were analyzed in the queen brain, subesophageal ganglion (SEG), and ovaries by immunofluorescence. Results suggest that the sNPF signaling cascade may be involved in diverse functions, and the sNPF peptide(s) may act in the brain and SEG as neurotransmitter(s) or neuromodulator(s), and in the ovaries as neurohormone(s). In addition, to elucidate the role of insulin signaling pathway in the fire ant, two putative InRs were cloned. Transcriptional expression analyses show that the receptor abundance was negatively correlated with body size and nutrition status in fire ant immatures. In queens, the expression of InRs in different queen tissues correlates with tissue requirements for queen reproductive physiology and behaviors. Advisors/Committee Members: Pietrantonio, Patricia V. (advisor), Vinson, S. Bradleigh (committee member), Coates, Craig (committee member), Carney, Ginger (committee member).

Subjects/Keywords: Fire ants; vitellogenin receptor; short neuropeptide F receptor; insulin receptor; queen reproduction

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APA (6^th Edition):

Lu, H. L. (2012). Vitellogenin Receptor and Neuropeptide Receptors Involved in Reproduction of the Red Imported Fire Ant (Solenopsis invicta Buren). (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2011-12-10218

Chicago Manual of Style (16^th Edition):

Lu, Hsiao Ling. “Vitellogenin Receptor and Neuropeptide Receptors Involved in Reproduction of the Red Imported Fire Ant (Solenopsis invicta Buren).” 2012. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021. http://hdl.handle.net/1969.1/ETD-TAMU-2011-12-10218.

MLA Handbook (7^th Edition):

Lu, Hsiao Ling. “Vitellogenin Receptor and Neuropeptide Receptors Involved in Reproduction of the Red Imported Fire Ant (Solenopsis invicta Buren).” 2012. Web. 03 Mar 2021.

Vancouver:

Lu HL. Vitellogenin Receptor and Neuropeptide Receptors Involved in Reproduction of the Red Imported Fire Ant (Solenopsis invicta Buren). [Internet] [Doctoral dissertation]. Texas A&M University; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2011-12-10218.

Council of Science Editors:

Lu HL. Vitellogenin Receptor and Neuropeptide Receptors Involved in Reproduction of the Red Imported Fire Ant (Solenopsis invicta Buren). [Doctoral Dissertation]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2011-12-10218

University of Toledo Health Science Campus

8. Wang, Mengjie. Brain Insulin-Like Growth Factor 1 Receptor and Insulin Receptor in Metabolism and Reproduction.

Degree: PhD, Biomedical Sciences (Molecular Medicine), 2019, University of Toledo Health Science Campus

URL: http://rave.ohiolink.edu/etdc/view?acc_num=mco1564676824418256

► Insulin-like growth factor 1 (IGF-1) and insulin exert biological effects through highly homologous tyrosine kinase receptors, which are ubiquitously expressed in rodents. During the last… (more)

▼ Insulin-like growth factor 1 (IGF-1) and insulin exert biological effects through highly homologous tyrosine kinase receptors, which are ubiquitously expressed in rodents. During the last two decades, substantial progress has been made in understanding the role of IGF-1 and insulin signaling in the brain. Major progress has been made in identifying differences of IGF-1 and insulin signaling in the brain and understanding the phenotypic discrepancies of disruptions of the IGF-1 receptors (IGF1Rs) and insulin receptors (IRs) in the brain. Metabolic diseases such as obesity and diabetes are global public health crises. Moreover, perturbations of metabolism cause various reproductive diseases such as abnormal puberty onset, irregular estrus cycle, altered ovarian function, infertility and reproductive system cancers. Thus, understanding and deciphering brain IGF1R and IR signaling are crucial to current research and crucial for potential therapeutic interventions for metabolic and reproductive diseases. Neurons are the fundamental units of the brain and carry out distinct functions, which raises another challenge – understanding the role of a given subset of neurons. Two subsets of neurons-leptin receptor (LepRb) neuron and kisspeptin (Kiss1) neuron have drawn my attention due to their distinct activities in metabolism and reproduction respectively. Current technique Cre/loxP system enables conditional suppression of gene expression in distinct subsets of neurons of interest. We used this technique to generate transgenic mice to study the role of IGF1R and IR signaling in LepRb neurons and Kiss1 neurons. Chapter 1 gives a review of metabolic and reproductive function of IGF1R and IR, and a central control of metabolism and reproduction by LepRb neurons and Kiss1 neurons. By characterizing reproductive and metabolic phenotype of mice lacking IGF1Rs and/or IRs exclusively in LepRb neurons (IGF1RLepRb mice and IGF1R/IRLepRb mice), we found that IGF1RLepRb and IGF1R/IRLepRb mice experienced growth retardation, delayed puberty and impaired fertility. Male mice had decreased gonadotropin and testosterone levels, impaired testicular histology, suggesting direct disruptions of hypothalamic-pituitary-gonadal axis. Interestingly, female reproductive hormones were normal at 4 weeks of age, while IGF1R/IRLepRb showed elevated gonadotropin and decreased follicle counts compared to female IGF1RLepRb or control mice. The decreased serum growth hormone (GH) and IGF-1 levels in male IGF1RLepRb mice demonstrates communication between LepRb neurons and the GH/IGF-1 axis. Our findings highlight the importance of IGF1R in LepRb neurons in the regulation of body growth, puberty and fertility (Chapter 2). In Chapter 3, we found female IGF1RLepRb mice had decreased body weight and food intake accompanied by increased VO2, physical activity, and thermogenic gene expression in brown adipose tissue (BAT). These effects were sexually dimorphic; IGF1R signaling was not critical in regulating body weight, food intake or glucose homeostasis in male… Advisors/Committee Members: Hill, Jennifer (Committee Chair).

Subjects/Keywords: Biomedical Research; Insulin-like growth factor 1 receptor; insulin receptor; leptin receptor-expressing neuron; kisspeptin neuron; metabolism; reproduction; gut micriobiota

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APA (6^th Edition):

Wang, M. (2019). Brain Insulin-Like Growth Factor 1 Receptor and Insulin Receptor in Metabolism and Reproduction. (Doctoral Dissertation). University of Toledo Health Science Campus. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=mco1564676824418256

Chicago Manual of Style (16^th Edition):

Wang, Mengjie. “Brain Insulin-Like Growth Factor 1 Receptor and Insulin Receptor in Metabolism and Reproduction.” 2019. Doctoral Dissertation, University of Toledo Health Science Campus. Accessed March 03, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=mco1564676824418256.

MLA Handbook (7^th Edition):

Wang, Mengjie. “Brain Insulin-Like Growth Factor 1 Receptor and Insulin Receptor in Metabolism and Reproduction.” 2019. Web. 03 Mar 2021.

Vancouver:

Wang M. Brain Insulin-Like Growth Factor 1 Receptor and Insulin Receptor in Metabolism and Reproduction. [Internet] [Doctoral dissertation]. University of Toledo Health Science Campus; 2019. [cited 2021 Mar 03]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1564676824418256.

Council of Science Editors:

Wang M. Brain Insulin-Like Growth Factor 1 Receptor and Insulin Receptor in Metabolism and Reproduction. [Doctoral Dissertation]. University of Toledo Health Science Campus; 2019. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1564676824418256

Univerzitet u Beogradu

9. Prodanović, Radiša, 1981-. Insulinska rezistencija kod krava Holštajn rase tokom perioda zasušenja i rane laktacije.

Degree: Fakultet veterinarske medicine, 2015, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:8045/bdef:Content/get

►

Veterinarska medicina - Bolesti papkara / Veterinary Medicine - Ruminants and Swine Diseases

Cilj istraživanja u okviru ove disertacije je bio da se ispita da… (more)

▼

Veterinarska medicina - Bolesti papkara / Veterinary Medicine - Ruminants and Swine Diseases

Cilj istraživanja u okviru ove disertacije je bio da se ispita da li u periodu oko teljenja postoje razlike u stepenu insulinske rezistencije kod visokomlečnih krava različite telesne kondicije. U tu svrhu je, 30. dana pre očekivanog teljenja, odabrano 16 krava holštajn rase različite telesne kondicije. Prvu grupu (kontrolna, n = 8) činile su krave optimalne telesne kondicije (ОТК = 3,00 до 3,25), a drugu (ogledna, n = 8) ugojene životinje (ОТК = 4,25 до 4,50). Sve životinje uključene u ogled podvrgnute su intravenskom testu opterećenja glukozom (GTT) četiri puta: 28. i 10. dana pre očekivanog termina teljenja, kao i 14. i 28. dana posle teljenja. Uzorci krvi su uzimani neposredno (0. minut) pre aplikacije rastvora glukoze, kao i 15., 30., 60., 90., 120. i 180. minuta nakon davanja glukoze. U uzorcima uzetim 0. minuta određivane su koncentracije ukupnih proteina, albumina, BHBA, ukupnog bilirubina, uree, Ca i P, dok je u svim uzetim uzorcima krvi određivana koncentracija glukoze, insulina i NEFA. Deset dana pre, kao i 14. dana posle teljenja uzeti su uzorci tkiva jetre, masnog i mišićnog tkiva od svih ispitanih životinja. U uzorcima tkiva jetre određivan je stepen zamašćenja jetre, a u uzorcima masnog tkiva dijametar adipocita. Zastupljenost proteina receptora za insulin i transportnog molekula za glukozu (GLUT 4) ispitana je u mišićnom i masnom tkivu. Za procenu stepena insulinske rezistencije tokom izvođenja GTT korišćeni su matematički izvedeni parametri metabolizma glukoze (k, T1/2, Pikgluk i AUCgluk), insulina (ΔMaxins, Pikins i AUCins), NEFA (AUCNEFA), kao i RQUICKY indeks. Rezultati su pokazali da antepartalno nije bilo značajne razlike u vrednostima ispitivanih biohemijskih parametara između dve grupe krava, dok je postpartalno utvrđena značajno viša koncentracija ukupnog bilirubina (p < 0,05) 14. dana, a značajno niža koncentracija albumina (p < 0,05) 28. dana laktacije kod oglednih u odnosu na kontrolne krave. Rezultati dobijeni tokom izvođenja prvog GTT su pokazali da je glikemija bila značajno veća (p < 0,05) kod oglednih nego kontrolnih krava jedino 180. minuta, dok se koncentracije insulina i NEFA nisu značajno razlikovale između dve grupe krava...°

Advisors/Committee Members: Šamanc, Horea, 1948-.

Subjects/Keywords: high-yielding dairy cows; body condition; insulin resistance; glucose tolerance test; insulin receptor; GLUT 4

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Prodanović, Radiša, 1. (2015). Insulinska rezistencija kod krava Holštajn rase tokom perioda zasušenja i rane laktacije. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:8045/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Prodanović, Radiša, 1981-. “Insulinska rezistencija kod krava Holštajn rase tokom perioda zasušenja i rane laktacije.” 2015. Thesis, Univerzitet u Beogradu. Accessed March 03, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:8045/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Prodanović, Radiša, 1981-. “Insulinska rezistencija kod krava Holštajn rase tokom perioda zasušenja i rane laktacije.” 2015. Web. 03 Mar 2021.

Vancouver:

Prodanović, Radiša 1. Insulinska rezistencija kod krava Holštajn rase tokom perioda zasušenja i rane laktacije. [Internet] [Thesis]. Univerzitet u Beogradu; 2015. [cited 2021 Mar 03]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:8045/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Prodanović, Radiša 1. Insulinska rezistencija kod krava Holštajn rase tokom perioda zasušenja i rane laktacije. [Thesis]. Univerzitet u Beogradu; 2015. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:8045/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Western Ontario

10. Oakie, Amanda. The role of c-Kit and insulin receptor tyrosine kinases in beta cell function and insulin secretion.

Degree: 2019, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/6232

► The receptor tyrosine kinases (RTKs) c-Kit and insulin receptor (IR) initiate similar intracellular signalling pathways in pancreatic beta cells to regulate beta cell proliferation, survival,… (more)

▼ The receptor tyrosine kinases (RTKs) c-Kit and insulin receptor (IR) initiate similar intracellular signalling pathways in pancreatic beta cells to regulate beta cell proliferation, survival, and insulin secretion. Mice with a c-Kit overexpression specifically in beta cells (c-KitβTg) demonstrated improved beta cell proliferation and insulin secretion compared to control mice, and islets from c-KitβTg mice also demonstrated increased IR expression. The potential interplay between c-Kit and IR and their roles during ageing and metabolic stress are not currently known. This work reports the examination of c-Kit and IR signalling using in vitro and in vivo models to determine their effects on beta cell proliferation and insulin secretion. To examine the effects of prolonged c-Kit signalling, c-KitβTg mice were analyzed at 60 weeks of age. The results from this section demonstrated that c-KitβTg mice developed impaired insulin release due to reduced soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) expression. Increased IR and phosphorylated IRS-1S612 and reduced insulin-induced Akt signalling were observed in islets from 60-week c-KitβTg mice. The effect of IR deficiency was examined by knocking down beta cell IR at 40 weeks in c-KitβTg mice and resulted in partial restoration of glucose tolerance. To determine the role of postnatal IR function on insulin secretion, a mouse model with beta cell-specific IR knockout (MIP-βIRKO) was generated and exposed to high-fat diet (HFD). MIP-βIRKO mice on HFD developed glucose intolerance due to reduced insulin secretion and SNARE expression. Islets from MIP-βIRKO HFD mice also demonstrated reduced Akt phosphorylation and GLUT2 levels. In vitro examination of INS-1 832/13 cells showed that co-stimulation of c-Kit and IR with ligands stem cell factor (SCF) and insulin, respectively, did not lead to synergistic intracellular signalling or proliferation when compared to single ligand treatments. This may be due to negative feedback from IRS-1S612 phosphorylation, which can be inhibited with rapamycin. In summary, this work presents a regulatory role for altered c-Kit and IR activity in maintaining beta cell intracellular signalling and insulin release. Results from these studies may be useful when considering RTK-based treatments to optimize islet function.

Subjects/Keywords: c-Kit; insulin receptor; diabetes mellitus; insulin secretion; SNARE protein; Cre recombinase; Endocrinology

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Oakie, A. (2019). The role of c-Kit and insulin receptor tyrosine kinases in beta cell function and insulin secretion. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/6232

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Oakie, Amanda. “The role of c-Kit and insulin receptor tyrosine kinases in beta cell function and insulin secretion.” 2019. Thesis, University of Western Ontario. Accessed March 03, 2021. https://ir.lib.uwo.ca/etd/6232.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Oakie, Amanda. “The role of c-Kit and insulin receptor tyrosine kinases in beta cell function and insulin secretion.” 2019. Web. 03 Mar 2021.

Vancouver:

Oakie A. The role of c-Kit and insulin receptor tyrosine kinases in beta cell function and insulin secretion. [Internet] [Thesis]. University of Western Ontario; 2019. [cited 2021 Mar 03]. Available from: https://ir.lib.uwo.ca/etd/6232.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Oakie A. The role of c-Kit and insulin receptor tyrosine kinases in beta cell function and insulin secretion. [Thesis]. University of Western Ontario; 2019. Available from: https://ir.lib.uwo.ca/etd/6232

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Arizona

11. Ananthakrishnan, Kameswari. Improved β-Cell Targeting and Therapeutics Using Multivalent Glucagon-Like Peptide-1 (GLP-1) Linked to the α2AR Antagonist Yohimbine (YHB): Evaluating the Binding, Selectivity and Signaling .

Degree: 2016, University of Arizona

URL: http://hdl.handle.net/10150/623004

► Diabetes Mellitus (DM) is a metabolic disorder in which the body fails to achieve glucose homeostasis, due to either insulin resistance or reduced insulin secretion… (more)

▼ Diabetes Mellitus (DM) is a metabolic disorder in which the body fails to achieve glucose homeostasis, due to either insulin resistance or reduced insulin secretion or both. This inadequate glucose control leads to hyperglycemia which, if left unchecked, leads to secondary complications like nephropathy, neuropathy, retinal degeneration and other serious conditions. In non-disease state, normal glucose level in the blood is maintained by pancreatic β-cells, which secrete insulin. However, during diabetes development, there is loss of β-cell mass and function; resulting in decreased insulin secretion which is the ultimate cause of hyperglycemia. The ability to non-invasively monitor changes in the β-cell mass during the development or treatment of diabetes would be a significant advance in diabetes management. However, a primary limitation for analysis of β-cell mass and developing dysfunction is the lack of specificity of β-cell targeting agents. Our novel approach for achieving the required specificity for a usable β-cell targeted contrast agent is to target a set of receptors on the cell surface that, as a combination, are unique to that cell. Through genetic screening, Glucagon Like Peptide-1 Receptor (GLP-1R) and α2Adrenergic Receptor (α2AR) were chosen as a potential molecular barcode for β-cells since their combination expression is relatively unique to the β-cells. GLP-1R and α2AR are both G-protein couple receptors (GPCRs) that, apart from being a β-cell specific combination, play an important role in regulating fundamental downstream signaling pathways in β-cells. To target these receptors effectively, we synthesized a multivalent ligand composed of Yohimbine (Yhb), an α2 adrenergic receptor (α2AR) antagonist, linked to an active Glucagon-like Peptide 1 analog (GLP-1₇₋₃₆). In this manuscript, I describe the synthesis and characterization of binding selectivity and signaling ability of GLP-1/Yhb at the cellular level. Using high throughput binding assays, we observed high affinity binding of GLP-1/Yhb to βTC3 cells, a β-cell mimetic line expressing both receptors, at a Kd of ~3 nM. Using microscopy, we observed significant Cy5-tagged GLP-1/Yhb binding and rapid internalization in cells expressing the complementary receptor pair at low concentrations, as low as 1 nM and 5 nM. When one of the receptors was made inaccessible due to presence of saturating quantities of a single unlabeled monomer, GLP-1/Yhb-Cy5 failed to bind to the cells at low concentrations (<10 nM). Similarly, in cells where either GLP-1R or α2AR were knocked down (using shRNA), binding of GLP-1/Yhb was significantly reduced (≤half of cells with both receptors), indicating strong selectivity of the ligand to cells expressing the combination of receptors. We also observed that GLP-1/Yhb construct modulates downstream signaling inβ TC3 cells resulting in enhanced Glucose Stimulated Insulin Secretion (GSIS). In presence of stimulatory glucose, GLP-1/Yhb significantly potentiated GSIS with a half-maximal effective dose of 2.6 nM. Compared to… Advisors/Committee Members: Lynch, Ronald (advisor), Lynch, Ronald (committeemember), Limesand, Sean (committeemember), Vagner, Josef (committeemember), Papas, Klearchos (committeemember).

Subjects/Keywords: GLP-1; Insulin secretion; Multivalency; Receptor targeting; β-cell imaging; Adrenergic receptor

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ananthakrishnan, K. (2016). Improved β-Cell Targeting and Therapeutics Using Multivalent Glucagon-Like Peptide-1 (GLP-1) Linked to the α2AR Antagonist Yohimbine (YHB): Evaluating the Binding, Selectivity and Signaling . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/623004

Chicago Manual of Style (16^th Edition):

Ananthakrishnan, Kameswari. “Improved β-Cell Targeting and Therapeutics Using Multivalent Glucagon-Like Peptide-1 (GLP-1) Linked to the α2AR Antagonist Yohimbine (YHB): Evaluating the Binding, Selectivity and Signaling .” 2016. Doctoral Dissertation, University of Arizona. Accessed March 03, 2021. http://hdl.handle.net/10150/623004.

MLA Handbook (7^th Edition):

Ananthakrishnan, Kameswari. “Improved β-Cell Targeting and Therapeutics Using Multivalent Glucagon-Like Peptide-1 (GLP-1) Linked to the α2AR Antagonist Yohimbine (YHB): Evaluating the Binding, Selectivity and Signaling .” 2016. Web. 03 Mar 2021.

Vancouver:

Ananthakrishnan K. Improved β-Cell Targeting and Therapeutics Using Multivalent Glucagon-Like Peptide-1 (GLP-1) Linked to the α2AR Antagonist Yohimbine (YHB): Evaluating the Binding, Selectivity and Signaling . [Internet] [Doctoral dissertation]. University of Arizona; 2016. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10150/623004.

Council of Science Editors:

Ananthakrishnan K. Improved β-Cell Targeting and Therapeutics Using Multivalent Glucagon-Like Peptide-1 (GLP-1) Linked to the α2AR Antagonist Yohimbine (YHB): Evaluating the Binding, Selectivity and Signaling . [Doctoral Dissertation]. University of Arizona; 2016. Available from: http://hdl.handle.net/10150/623004

University of Pretoria

12. Hughes, Stephen Bernard. Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue .

Degree: 2012, University of Pretoria

URL: http://upetd.up.ac.za/thesis/available/etd-08082012-144801/

► has been significant progress in the development of new technologies and methodologies to characterize gene expression. The fluorescent-based real-time reverse transcription (RT) polymerase chain reaction… (more)

▼ has been significant progress in the development of new technologies and methodologies to characterize gene expression. The fluorescent-based real-time reverse transcription (RT) polymerase chain reaction (PCR) is an important tool used for clinical and molecular research, biotechnology and as a diagnostic test. Insulin-like growth factors (IGF-1 and IGF-2) and insulin are ubiquitously expressed and play important roles in the regulation of cell growth, differentiation and the maintenance of cell differentiation in mammals. The IGF system (IGF-1, IGF-2, IGF -1 receptor, IGF-2 receptor and six IGF-binding proteins) and insulin are consequently essential to most aspects of male and female reproduction. IGF-1 is produced in multiple tissues but predominately in the liver, from where it enters the circulation. Insulin is secreted by β-cells of the pancreas’ islets of Langerhans. Both IGF-1 and insulin polypeptides bind to specific cell surface receptors. These receptors are members of the superfamily known as tyrosine protein kinases, and are composed of two α and two β subunits linked by disulfide bonds to form an αβ–αβ heterotetramer. The α subunits include ligand binding sites, whereas the β subunits contain tyrosine kinase activity. The aim of this project was to develop real-time RT-PCR assays for quantification of equine insulin-like growth factor-1 receptor (IGF-1R) and insulin receptor (INS-R) mRNA. The assays were developed using stallion testicular tissue samples, obtained by excisional biopsy, from three horse breeds (Friesan, Thoroughbred and Warmblood). The assays developed were efficient, sensitive and had a broad linear range of detection (seven logs for IGF-1R and six logs for INS-R). The assays worked well in our hands and were both sensitive and specific for the detection of equine IGF-1R and INS-R mRNA in a variety of equine tissues. Advisors/Committee Members: Schulman, Martin L (advisor), Guthrie, Alan John (advisor), Quan, Melvyn (advisor).

Subjects/Keywords: Insulin receptor; UCTD; Equine tissue; Transcription polymerase; Tyrosine protein kinases

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❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hughes, S. B. (2012). Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue . (Masters Thesis). University of Pretoria. Retrieved from http://upetd.up.ac.za/thesis/available/etd-08082012-144801/

Chicago Manual of Style (16^th Edition):

Hughes, Stephen Bernard. “Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue .” 2012. Masters Thesis, University of Pretoria. Accessed March 03, 2021. http://upetd.up.ac.za/thesis/available/etd-08082012-144801/.

MLA Handbook (7^th Edition):

Hughes, Stephen Bernard. “Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue .” 2012. Web. 03 Mar 2021.

Vancouver:

Hughes SB. Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue . [Internet] [Masters thesis]. University of Pretoria; 2012. [cited 2021 Mar 03]. Available from: http://upetd.up.ac.za/thesis/available/etd-08082012-144801/.

Council of Science Editors:

Hughes SB. Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue . [Masters Thesis]. University of Pretoria; 2012. Available from: http://upetd.up.ac.za/thesis/available/etd-08082012-144801/

University of Utah

13. Komanetsky, Susan M. Characterization of retinol binding protein receptor 2, a putative retinol transporter and serum retinol binding protein receptor.

Degree: MS, Nutrition, 2013, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/2302/rec/432

► min A (retinol) is essential for life; however, little is known about how it istransported into cells. Ninety-five percent of retinol found in blood is… (more)

Subjects/Keywords: Insulin resistance; RBP4; RBP4 receptor; Retinol; Retinol homeostasis; Retinol transport

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Komanetsky, S. M. (2013). Characterization of retinol binding protein receptor 2, a putative retinol transporter and serum retinol binding protein receptor. (Masters Thesis). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/2302/rec/432

Chicago Manual of Style (16^th Edition):

Komanetsky, Susan M. “Characterization of retinol binding protein receptor 2, a putative retinol transporter and serum retinol binding protein receptor.” 2013. Masters Thesis, University of Utah. Accessed March 03, 2021. http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/2302/rec/432.

MLA Handbook (7^th Edition):

Komanetsky, Susan M. “Characterization of retinol binding protein receptor 2, a putative retinol transporter and serum retinol binding protein receptor.” 2013. Web. 03 Mar 2021.

Vancouver:

Komanetsky SM. Characterization of retinol binding protein receptor 2, a putative retinol transporter and serum retinol binding protein receptor. [Internet] [Masters thesis]. University of Utah; 2013. [cited 2021 Mar 03]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/2302/rec/432.

Council of Science Editors:

Komanetsky SM. Characterization of retinol binding protein receptor 2, a putative retinol transporter and serum retinol binding protein receptor. [Masters Thesis]. University of Utah; 2013. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/2302/rec/432

14. Landis, Justine M. Mechanistic Analysis of Differential Signal Transduction Mediated by the Insulin Receptor Substrate Proteins IRS-1 and IRS-2: A Dissertation.

Degree: Cancer Biology, Molecular, Cell and Cancer Biology Department, 2014, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/735

► The Insulin Receptor Substrate (IRS) proteins IRS-1 and IRS-2 are cytoplasmic adaptor proteins that organize and propagate intracellular signaling downstream of specific growth factor… (more)

Subjects/Keywords: Signal Transduction; Insulin Receptor Substrate Proteins; Biochemistry; Cancer Biology

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❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Landis, J. M. (2014). Mechanistic Analysis of Differential Signal Transduction Mediated by the Insulin Receptor Substrate Proteins IRS-1 and IRS-2: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/735

Chicago Manual of Style (16^th Edition):

Landis, Justine M. “Mechanistic Analysis of Differential Signal Transduction Mediated by the Insulin Receptor Substrate Proteins IRS-1 and IRS-2: A Dissertation.” 2014. Doctoral Dissertation, U of Massachusetts : Med. Accessed March 03, 2021. http://escholarship.umassmed.edu/gsbs_diss/735.

MLA Handbook (7^th Edition):

Landis, Justine M. “Mechanistic Analysis of Differential Signal Transduction Mediated by the Insulin Receptor Substrate Proteins IRS-1 and IRS-2: A Dissertation.” 2014. Web. 03 Mar 2021.

Vancouver:

Landis JM. Mechanistic Analysis of Differential Signal Transduction Mediated by the Insulin Receptor Substrate Proteins IRS-1 and IRS-2: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2014. [cited 2021 Mar 03]. Available from: http://escholarship.umassmed.edu/gsbs_diss/735.

Council of Science Editors:

Landis JM. Mechanistic Analysis of Differential Signal Transduction Mediated by the Insulin Receptor Substrate Proteins IRS-1 and IRS-2: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2014. Available from: http://escholarship.umassmed.edu/gsbs_diss/735

Vanderbilt University

15. Ustione, Alessandro. Dopaminergic regulation of insulin secretion from the pancreatic islet.

Degree: PhD, Molecular Physiology and Biophysics, 2012, Vanderbilt University

URL: http://hdl.handle.net/1803/14923

► Insulin secretion is the natural response to hyperglycemia, and it is crucial to maintain glucose homeostasis in healthy individuals. Impairment in this regulation eventually results… (more)

Subjects/Keywords: pancreatic islet; dopamine; dopamine receptor; dopamine transporter; diabetes; insulin secretion

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ustione, A. (2012). Dopaminergic regulation of insulin secretion from the pancreatic islet. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14923

Chicago Manual of Style (16^th Edition):

Ustione, Alessandro. “Dopaminergic regulation of insulin secretion from the pancreatic islet.” 2012. Doctoral Dissertation, Vanderbilt University. Accessed March 03, 2021. http://hdl.handle.net/1803/14923.

MLA Handbook (7^th Edition):

Ustione, Alessandro. “Dopaminergic regulation of insulin secretion from the pancreatic islet.” 2012. Web. 03 Mar 2021.

Vancouver:

Ustione A. Dopaminergic regulation of insulin secretion from the pancreatic islet. [Internet] [Doctoral dissertation]. Vanderbilt University; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1803/14923.

Council of Science Editors:

Ustione A. Dopaminergic regulation of insulin secretion from the pancreatic islet. [Doctoral Dissertation]. Vanderbilt University; 2012. Available from: http://hdl.handle.net/1803/14923

University of Pretoria

16. Hughes, Stephen Bernard. Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue.

Degree: Production Animal Studies, 2011, University of Pretoria

URL: http://hdl.handle.net/2263/31135

► has been significant progress in the development of new technologies and methodologies to characterize gene expression. The fluorescent-based real-time reverse transcription (RT) polymerase chain reaction… (more)

▼ has been significant progress in the development of new technologies and methodologies to characterize gene expression. The fluorescent-based real-time reverse transcription (RT) polymerase chain reaction (PCR) is an important tool used for clinical and molecular research, biotechnology and as a diagnostic test. Insulin-like growth factors (IGF-1 and IGF-2) and insulin are ubiquitously expressed and play important roles in the regulation of cell growth, differentiation and the maintenance of cell differentiation in mammals. The IGF system (IGF-1, IGF-2, IGF -1 receptor, IGF-2 receptor and six IGF-binding proteins) and insulin are consequently essential to most aspects of male and female reproduction. IGF-1 is produced in multiple tissues but predominately in the liver, from where it enters the circulation. Insulin is secreted by β-cells of the pancreas’ islets of Langerhans. Both IGF-1 and insulin polypeptides bind to specific cell surface receptors. These receptors are members of the superfamily known as tyrosine protein kinases, and are composed of two α and two β subunits linked by disulfide bonds to form an αβ–αβ heterotetramer. The α subunits include ligand binding sites, whereas the β subunits contain tyrosine kinase activity. The aim of this project was to develop real-time RT-PCR assays for quantification of equine insulin-like growth factor-1 receptor (IGF-1R) and insulin receptor (INS-R) mRNA. The assays were developed using stallion testicular tissue samples, obtained by excisional biopsy, from three horse breeds (Friesan, Thoroughbred and Warmblood). The assays developed were efficient, sensitive and had a broad linear range of detection (seven logs for IGF-1R and six logs for INS-R). The assays worked well in our hands and were both sensitive and specific for the detection of equine IGF-1R and INS-R mRNA in a variety of equine tissues. Advisors/Committee Members: Schulman, Martin L. (advisor), Guthrie, Alan John (coadvisor), Quan, Melvyn (coadvisor).

Subjects/Keywords: Insulin receptor; UCTD; Equine tissue; Transcription polymerase; Tyrosine protein kinases

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hughes, S. B. (2011). Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue. (Masters Thesis). University of Pretoria. Retrieved from http://hdl.handle.net/2263/31135

Chicago Manual of Style (16^th Edition):

Hughes, Stephen Bernard. “Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue.” 2011. Masters Thesis, University of Pretoria. Accessed March 03, 2021. http://hdl.handle.net/2263/31135.

MLA Handbook (7^th Edition):

Hughes, Stephen Bernard. “Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue.” 2011. Web. 03 Mar 2021.

Vancouver:

Hughes SB. Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue. [Internet] [Masters thesis]. University of Pretoria; 2011. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2263/31135.

Council of Science Editors:

Hughes SB. Development of real-time reverse transcription polymerase chain reaction assays to quantify insulin-like growth factor-1 receptor and insulin receptor expression in equine tissue. [Masters Thesis]. University of Pretoria; 2011. Available from: http://hdl.handle.net/2263/31135

Harvard University

17. Green, Delbert Andre. Developmental and Genetic Mechanisms of Ovariole Number Evolution in Drosophila.

Degree: PhD, Biology, Molecular and Cellular, 2014, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:12274190

► The goal of the "Quantitative Trait Gene" (QTG) program is to identify genes and mutations that underlie natural phenotypic variation. My goal with this work… (more)

▼ The goal of the "Quantitative Trait Gene" (QTG) program is to identify genes and mutations that underlie natural phenotypic variation. My goal with this work was to contribute an additional model to the program: ovariole number evolution in Drosophila. In this thesis I describe the progress I have made towards identifying a specific genetic change that contributed to the divergence of ovariole number between two Drosophila lineages. I identify specific developmental mechanisms relevant to establishing ovariole number in different Drosophila lineages by detailing ovarian cell-type specific specification, proliferation, and differentiation. I test specific candidates of genetic regulators of these developmental mechanisms with mutational analysis in D. melanogaster. I show that independent evolution of ovariole number has resulted from changes in distinct developmental mechanisms, each of which may have a different underlying genetic basis in Drosophila. I use the interspecies comparison of D. melanogaster versus D. sechellia to test for functional differences in insulin/insulin-like growth factor (IIS) signaling between the two species. I show that IIS activity levels and sensitivity have diverged between species, leading to both species-specific ovariole number and species-specific nutritional plasticity in ovariole number. Moreover, plastic range of ovariole number correlates with ecological niche, suggesting that the degree of nutritional plasticity may be an adaptive trait. My work and quantitative genetic analyses strongly support the hypothesis that evolution of the Drosophila insulin-like receptor (InR) gene, specifically, is at least partially responsible for the divergence in ovariole number and nutritional plasticity of ovariole number between D. melanogaster and D. sechellia. I detail ongoing experiments to test this hypothesis explicitly via cross-species transgenesis. Advisors/Committee Members: Extavour, Cassandra G. (advisor), Mango, Susan (committee member), Hoekstra, Hopi (committee member), Perrimon, Norbert (committee member).

Subjects/Keywords: Biology; convergent evolution; Drosophila; Insulin Receptor; ovariole; plasticity

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Green, D. A. (2014). Developmental and Genetic Mechanisms of Ovariole Number Evolution in Drosophila. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:12274190

Chicago Manual of Style (16^th Edition):

Green, Delbert Andre. “Developmental and Genetic Mechanisms of Ovariole Number Evolution in Drosophila.” 2014. Doctoral Dissertation, Harvard University. Accessed March 03, 2021. http://nrs.harvard.edu/urn-3:HUL.InstRepos:12274190.

MLA Handbook (7^th Edition):

Green, Delbert Andre. “Developmental and Genetic Mechanisms of Ovariole Number Evolution in Drosophila.” 2014. Web. 03 Mar 2021.

Vancouver:

Green DA. Developmental and Genetic Mechanisms of Ovariole Number Evolution in Drosophila. [Internet] [Doctoral dissertation]. Harvard University; 2014. [cited 2021 Mar 03]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:12274190.

Council of Science Editors:

Green DA. Developmental and Genetic Mechanisms of Ovariole Number Evolution in Drosophila. [Doctoral Dissertation]. Harvard University; 2014. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:12274190

University of Toronto

18. Bansal, Pritpal. Insulin-induced Suppression of A-type GABA Receptor Signaling in the INS-1 Pancreatic β-cell Line.

Degree: 2010, University of Toronto

URL: http://hdl.handle.net/1807/25419

►

GABA and GABA type A receptor (GABAAR) are expressed in pancreatic β-cells and comprise an autocrine signaling system. How the GABA-GABAAR system is regulated is… (more)

Subjects/Keywords: GABA; Insulin; Beta-cell; Autocrine; GABA receptor; Islet; Electrophysiology; 0719

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APA (6^th Edition):

Bansal, P. (2010). Insulin-induced Suppression of A-type GABA Receptor Signaling in the INS-1 Pancreatic β-cell Line. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/25419

Chicago Manual of Style (16^th Edition):

Bansal, Pritpal. “Insulin-induced Suppression of A-type GABA Receptor Signaling in the INS-1 Pancreatic β-cell Line.” 2010. Masters Thesis, University of Toronto. Accessed March 03, 2021. http://hdl.handle.net/1807/25419.

MLA Handbook (7^th Edition):

Bansal, Pritpal. “Insulin-induced Suppression of A-type GABA Receptor Signaling in the INS-1 Pancreatic β-cell Line.” 2010. Web. 03 Mar 2021.

Vancouver:

Bansal P. Insulin-induced Suppression of A-type GABA Receptor Signaling in the INS-1 Pancreatic β-cell Line. [Internet] [Masters thesis]. University of Toronto; 2010. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1807/25419.

Council of Science Editors:

Bansal P. Insulin-induced Suppression of A-type GABA Receptor Signaling in the INS-1 Pancreatic β-cell Line. [Masters Thesis]. University of Toronto; 2010. Available from: http://hdl.handle.net/1807/25419

AUT University

19. Jain, Reema. When too much sun is never enough: association of the VDR gene polymorphisms with insulin resistance .

Degree: 2010, AUT University

URL: http://hdl.handle.net/10292/990

► The metabolism of vitamin D commences with exposure of the skin to sunlight. The growing recognition of its role in insulin resistance, autoimmune disorders, infections,… (more)

▼ The metabolism of vitamin D commences with exposure of the skin to sunlight. The growing recognition of its role in insulin resistance, autoimmune disorders, infections, cancer, as well as the health of cells that influence physical and mental function have profound implications on how we define vitamin D requirements and why we should care whether they are met or not. Most of the actions of vitamin D are mediated by the vitamin D receptor (VDR), a protein whose gene sequence can vary, giving rise to polymorphic forms which are potent enough to affect the binding capacity of this protein to vitamin D. Some of these polymorphic forms of VDR gene may be associated with reduced effectiveness of vitamin D and hence predispose individuals to diseases such as type 2 diabetes and insulin resistance. An earlier study, the Surya Study, looked at the responsiveness of the South-Asian women living in Auckland to vitamin D. The research described here is an extension of this study and its focus was to identify the associations/linkages between certain polymorphic forms of the VDR gene and the disease conditions and intervention responsiveness in the same women. The first objective was to compare two well known techniques for genotyping single nucleotide polymorphisms (SNPs) of the VDR gene at the 3’ end, namely BsmI, ApaI and TaqI: the newer real-time polymerase chain reaction (qPCR) and the traditional restriction fragment length polymorphism polymerase chain reaction (RFLP-PCR) techniques. This comparison was performed to evaluate alternative methods for genotyping which consumed less time than RFLP-PCR. When the presence of each polymorphism by both the techniques was compared in this cohort of South-Asian women, it was found that RFLP-PCR proved to be a more reliable technique than qPCR for genotyping the VDR gene. Another objective of this project was to investigate the prevalence of the above three polymorphisms along with Cdx-2 and FokI SNPs which are present at the 5’ end of the VDR gene, in the population under study and their possible association with phenotypes such as vitamin D responsiveness and insulin resistance. These women were screened and biochemical data was collected during the earlier Surya Study. Of these, eighty-one women were then selected for intervention based on them having high insulin resistance (HOMA-IR>1.93) and serum 25(OH)D<50 nmol/L. Out of these eighty-one women, forty-two were given vitamin D supplement and thirty-nine were given a placebo for six months. Baseline and endpoint measurements included insulin resistance (HOMA-IR), insulin sensitivity (HOMA2%S) etc. How each individual responded to treatment in the intervention group was analysed in the context of the polymorphisms that they had. An association of insulin resistance with BsmI, ApaI and TaqI SNPs was observed in this cohort of 239 women. The response to insulin resistance in the vitamin D supplemented group significantly differed for FokI genotype compared to other genotypes. This explained why certain women responded to treatment… Advisors/Committee Members: Higgins, Colleen (advisor), Love, Donald (advisor).

Subjects/Keywords: Vitamin D receptor; Polymorphisms; Haplotype; Association; Insulin resistance; RFLP-PCR

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APA (6^th Edition):

Jain, R. (2010). When too much sun is never enough: association of the VDR gene polymorphisms with insulin resistance . (Thesis). AUT University. Retrieved from http://hdl.handle.net/10292/990

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Jain, Reema. “When too much sun is never enough: association of the VDR gene polymorphisms with insulin resistance .” 2010. Thesis, AUT University. Accessed March 03, 2021. http://hdl.handle.net/10292/990.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Jain, Reema. “When too much sun is never enough: association of the VDR gene polymorphisms with insulin resistance .” 2010. Web. 03 Mar 2021.

Vancouver:

Jain R. When too much sun is never enough: association of the VDR gene polymorphisms with insulin resistance . [Internet] [Thesis]. AUT University; 2010. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10292/990.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Jain R. When too much sun is never enough: association of the VDR gene polymorphisms with insulin resistance . [Thesis]. AUT University; 2010. Available from: http://hdl.handle.net/10292/990

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Southern California

20. Mangahas, Ana Marie E. The possible aberrant function of MBNL1 with insulin receptor (IR-B) mRNA in myotonic dystrophy type I.

Degree: MS, Biochemistry & Molecular Biology, 2007, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/156892/rec/7111

► Myotonic Dystrophy (DM) a multi-systemic disorder, is the most common adult muscular dystrophy form. Among the pathological manifestations observed in the skeletal musculature include non-muscle… (more)

Subjects/Keywords: Myotonic Dystrophy; insulin receptor

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APA (6^th Edition):

Mangahas, A. M. E. (2007). The possible aberrant function of MBNL1 with insulin receptor (IR-B) mRNA in myotonic dystrophy type I. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/156892/rec/7111

Chicago Manual of Style (16^th Edition):

Mangahas, Ana Marie E. “The possible aberrant function of MBNL1 with insulin receptor (IR-B) mRNA in myotonic dystrophy type I.” 2007. Masters Thesis, University of Southern California. Accessed March 03, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/156892/rec/7111.

MLA Handbook (7^th Edition):

Mangahas, Ana Marie E. “The possible aberrant function of MBNL1 with insulin receptor (IR-B) mRNA in myotonic dystrophy type I.” 2007. Web. 03 Mar 2021.

Vancouver:

Mangahas AME. The possible aberrant function of MBNL1 with insulin receptor (IR-B) mRNA in myotonic dystrophy type I. [Internet] [Masters thesis]. University of Southern California; 2007. [cited 2021 Mar 03]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/156892/rec/7111.

Council of Science Editors:

Mangahas AME. The possible aberrant function of MBNL1 with insulin receptor (IR-B) mRNA in myotonic dystrophy type I. [Masters Thesis]. University of Southern California; 2007. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/156892/rec/7111

University of New South Wales

21. Pedersen , David. The role of protein kinase C ε in insulin receptor trafficking and insulin action.

Degree: Clinical School - St Vincent's Hospital, 2012, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/51788 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10455/SOURCE02?view=true

► The development of type 2 diabetes is reaching epidemic proportions and identifying ways to modulate insulin levels in order to maintain euglycaemia is important in… (more)

▼ The development of type 2 diabetes is reaching epidemic proportions and identifying ways to modulate insulin levels in order to maintain euglycaemia is important in understanding how to better treat this disease. It is now accepted that lipid oversupply can detrimentally affect insulin action and the lipid activated kinase, protein kinase C epsilon (PKCε), has been implicated in the development of insulin resistance and progression to type 2 diabetes. We have previously shown that global PKCε knockout (PKCε KO) mice are protected from high fat diet induced glucose intolerance, in part through reduced hepatic insulin clearance.We have shown using wild type (WT) and PKCε KO mouse embryonic fibroblasts (MEFs) as a model that ablation of PKCε perturbs insulin uptake and this was associated with a reduction in insulin-stimulated insulin receptor (InsR) redistribution within the cell, by subcellular fractionation. This was associated with a differential localisation of the InsR in the basal state in PKCε KO MEFs, with a greater proportion of the IR localised to cellular lipid microdomains. Insulin-stimulated InsR tyrosine phosphorylation within the kinase domain at sites 1162/1163 was reduced, however this defect in InsR phosphorylation did not translate to defective downstream signalling, with insulin-stimulated PKCε KO MEFs having normal or enhanced Akt/PKB, Erk1/2 and IRS-1 phosphorylation. Potential mechanisms for these differences were investigated by examining key candidates such as expression of the InsR substrate, Ceacam1 and the docking protein Grb14, to deduce the effect upon InsR internalisation and signalling, with Ceacam1 expression found to be greatly reduced in PKCε KO MEFs. Insulin signalling was further investigated in primary hepatocytes and in vivo following stimulation of de novo insulin secretion to examine these findings in more physiological settings.The role of PKCε in lipid-induced insulin resistance was also investigated as PKCε has been shown to affect lipid metabolism. The incorporation of the fatty acid palmitate into distinct lipid classes was examined, as alterations in cellular lipid composition could contribute to alterations in insulin action, however no major changes were observed. However, following palmitate treatment of MEFs, PKCε KO MEFs displayed a greater preservation of downstream insulin signalling compared to WT MEFs. The data is consistent with a role for PKCε in the generation of insulin resistance through the modulation of lipid metabolism, rather than merely acting downstream of specific lipid intermediates. Advisors/Committee Members: Schmitz-Peiffer, Carsten, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW.

Subjects/Keywords: Insulin Receptor; Protein Kinase C epsilon; Ceacam1; Trafficking; Signalling

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pedersen , D. (2012). The role of protein kinase C ε in insulin receptor trafficking and insulin action. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/51788 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10455/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Pedersen , David. “The role of protein kinase C ε in insulin receptor trafficking and insulin action.” 2012. Doctoral Dissertation, University of New South Wales. Accessed March 03, 2021. http://handle.unsw.edu.au/1959.4/51788 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10455/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Pedersen , David. “The role of protein kinase C ε in insulin receptor trafficking and insulin action.” 2012. Web. 03 Mar 2021.

Vancouver:

Pedersen D. The role of protein kinase C ε in insulin receptor trafficking and insulin action. [Internet] [Doctoral dissertation]. University of New South Wales; 2012. [cited 2021 Mar 03]. Available from: http://handle.unsw.edu.au/1959.4/51788 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10455/SOURCE02?view=true.

Council of Science Editors:

Pedersen D. The role of protein kinase C ε in insulin receptor trafficking and insulin action. [Doctoral Dissertation]. University of New South Wales; 2012. Available from: http://handle.unsw.edu.au/1959.4/51788 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10455/SOURCE02?view=true

Universiteit Utrecht

22. Wilms, A.T. Protein expression of insuline-like growth factor I and II, growth hormone and growth hormone receptor in canine cortisol-producing adrenocortical tumors.

Degree: 2012, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/289411

► Cushing’s syndrome is an important endocrinological disorder in dogs. In 15-20% of the cases it is caused by excessive secretion of glucocorticoids by an adrenocortical… (more)

Subjects/Keywords: Cushing's syndrome; adrenocortical tumor; cortisol-producing adrenocortical ademonas; cortisol-producing adrenocortical carcinomas; growth hormone; growth hormone receptor; insulin-like growth factor I receptor; insulin-like growth factor II receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wilms, A. T. (2012). Protein expression of insuline-like growth factor I and II, growth hormone and growth hormone receptor in canine cortisol-producing adrenocortical tumors. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/289411

Chicago Manual of Style (16^th Edition):

Wilms, A T. “Protein expression of insuline-like growth factor I and II, growth hormone and growth hormone receptor in canine cortisol-producing adrenocortical tumors.” 2012. Doctoral Dissertation, Universiteit Utrecht. Accessed March 03, 2021. http://dspace.library.uu.nl:8080/handle/1874/289411.

MLA Handbook (7^th Edition):

Wilms, A T. “Protein expression of insuline-like growth factor I and II, growth hormone and growth hormone receptor in canine cortisol-producing adrenocortical tumors.” 2012. Web. 03 Mar 2021.

Vancouver:

Wilms AT. Protein expression of insuline-like growth factor I and II, growth hormone and growth hormone receptor in canine cortisol-producing adrenocortical tumors. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2012. [cited 2021 Mar 03]. Available from: http://dspace.library.uu.nl:8080/handle/1874/289411.

Council of Science Editors:

Wilms AT. Protein expression of insuline-like growth factor I and II, growth hormone and growth hormone receptor in canine cortisol-producing adrenocortical tumors. [Doctoral Dissertation]. Universiteit Utrecht; 2012. Available from: http://dspace.library.uu.nl:8080/handle/1874/289411

University of Georgia

23. Castillo, Julio Cesar. Spatio-temporal characterization of the insulin signaling cascade and its role in regulating hemocyte proliferation in Aedes aegypti.

Degree: 2014, University of Georgia

URL: http://hdl.handle.net/10724/26864

► Hemocytes are central for cell based immunity. In this study, I compared an improved technique (this study) to collect hemocytes from mosquitoes to other welle… (more)

▼ Hemocytes are central for cell based immunity. In this study, I compared an improved technique (this study) to collect hemocytes from mosquitoes to other welle stablished methods. Collection method greatly affected the number of hemocytes and contaminants obtained from adult females of each species. Using a collection method called high injection/recovery I was able to show that hemolymph from An. gambiae and Ae. aegypti adult females contains three hemocyte types (granulocytes, oenocytoids and prohemocytes) that were distinguished from one another by a combination of morphological and functional markers. Granulocytes were the most abundant cell type in both species while oenocytoids and prohemocytes comprised less than 10% of the total hemocyte population. The number of hemocytes recovered from sugar fed females declined with age but blood feeding transiently increased hemocyte abundance. In order to understand the nature of the increase in blood cells after a blood meal, the role of insulin signaling as key regulator of cell proliferation was investigated. Several brain-specific ILPs (-3, -4, -7, and -8) were found to be expressed in hemocytes, and their expression pattern differ between blood fed and non-blood fed female mosquitoes. Experiments showed that decapitated females exhibited no increase in hemocyte abundance. ILP-3 injected into blood fed/decapitated females rescued the observed cell increase phenotype, and hemocyte increase was restored. BrdU labeling of hemocytes showed that blood fed females had higher numbers of BrdU positive cells when compared to non blood fed controls, indicating that blood feeding stimulates cell proliferation. RNAi knock down using dsRNA targeting the mosquito insulin receptor (MIR) inhibited hemocyte increases. Additionally, the total hemocyte number in dsRNA-MIR treated blood fed and non-blood fed females was considerably lower, suggesting that ILPs may also serve as a survival signal. Lastly I found that the increase in hemocyte numbers observed in blood fed animals confered resistance to bacterial infection.

Subjects/Keywords: insulin-like peptides; ILP; hemocytes; MIR; insulin receptor; mosquito; Aedes aegypti; Anopheles gambiae; Drosophila melanogaster; cell proliferation.

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APA (6^th Edition):

Castillo, J. C. (2014). Spatio-temporal characterization of the insulin signaling cascade and its role in regulating hemocyte proliferation in Aedes aegypti. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/26864

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Castillo, Julio Cesar. “Spatio-temporal characterization of the insulin signaling cascade and its role in regulating hemocyte proliferation in Aedes aegypti.” 2014. Thesis, University of Georgia. Accessed March 03, 2021. http://hdl.handle.net/10724/26864.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Castillo, Julio Cesar. “Spatio-temporal characterization of the insulin signaling cascade and its role in regulating hemocyte proliferation in Aedes aegypti.” 2014. Web. 03 Mar 2021.

Vancouver:

Castillo JC. Spatio-temporal characterization of the insulin signaling cascade and its role in regulating hemocyte proliferation in Aedes aegypti. [Internet] [Thesis]. University of Georgia; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10724/26864.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Castillo JC. Spatio-temporal characterization of the insulin signaling cascade and its role in regulating hemocyte proliferation in Aedes aegypti. [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/26864

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

24. Reiter, Chad. Constitutive insulin receptor signaling in retina and changes induced by diabetes .

Degree: 2008, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/6379

► Diabetes is a growing epidemic in Western society which afflicts over 17 million Americans and over 151 million people world wide. People with diabetes are… (more)

▼ Diabetes is a growing epidemic in Western society which afflicts over 17 million Americans and over 151 million people world wide. People with diabetes are at a greater risk of developing vascular complications such as atherosclerosis, stroke, and heart failure, as well as complications in specific tissues such as nephropathy and kidney failure, neuropathy and amputation of extremities, and retinopathy and blindness. Diabetic retinopathy (DR) is the leading cause of blindness in working age adults, and it is diagnosed by visual inspection of vascular alterations in the retina. Over time, the retinal blood vessels become leaky and undergo neovascularization. This leaking leads to macular edema, hemorrhaging, and build-up of opaque exudates, and the neovascularization causes severe loss of vision due to vitreous hemorrhages and/or retinal detachment. Currently, the only treatment for DR is laser ablation of the growing and leaky vessels. The procedure temporarily slows the abnormal blood vessel growth, but this ¡§amputation¡¨ procedure also damages the neural retina, and patients often require numerous treatments. In addition to vascular abnormalities in DR, the neural retina also is affected by diabetes, and apoptosis is increased in the neural retina of diabetic rats and humans. Clearly, alternative treatments are necessary to slow and prevent DR to preserve vision. In a general sense, diabetes is a disease of improper insulin action leading to hyperglycemia. Insulin causes many cell-signaling events to occur through the insulin receptor (IR) to promote glucose uptake, but insulin also generates a cellular survival signal which is mediated by the protein kinase Akt. While hyperglycemia has been assumed to be the major factor that promotes diabetic complications, and despite the current knowledge of insulin signal transduction on tissues that directly mediate nutrient storage, relatively little is known about insulin physiology and the effects of diabetes in complication-prone tissues, such as the retina. Therefore, the focus of this project is to elucidate proximal IR signaling and its regulation of Akt in retina tissue, and to test the hypothesis that the retina, similar to other classical insulin target tissues, has insulin signaling defects with diabetes. This work provides a better understanding of mechanisms which may contribute to apoptosis in the diseased retina. The first specific aim of this project was to determine the early IR signaling events, and to test the hypothesis that retinal insulin receptors are active in vivo. When insulin was injected systemically into fasting rats, muscle insulin receptor ƒÒ subunit (IRƒÒ) autophosphorylation on tyrosine residues significantly increased within five minutes, but retinal IRƒÒ autophosphorylation did not increase until 30 minutes after the injection. Furthermore, the insulin injection increased Akt phosphorylation on serine 473 in retina. Interestingly, it was determined that the basal IR and Akt-1 kinase activities were elevated in retina… Advisors/Committee Members: Thomas Wright Gardner, Committee Chair/Co-Chair, David A Antonetti, Committee Member, Scot R Kimball, Committee Member, Charles H Lang, Committee Member, Kathryn F Lanoue, Committee Member, Ian Alexander Simpson, Committee Member.

Subjects/Keywords: insulin receptor; diabetic retinopathy; retina; insulin; signal transduction

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Reiter, C. (2008). Constitutive insulin receptor signaling in retina and changes induced by diabetes . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/6379

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Reiter, Chad. “Constitutive insulin receptor signaling in retina and changes induced by diabetes .” 2008. Thesis, Penn State University. Accessed March 03, 2021. https://submit-etda.libraries.psu.edu/catalog/6379.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Reiter, Chad. “Constitutive insulin receptor signaling in retina and changes induced by diabetes .” 2008. Web. 03 Mar 2021.

Vancouver:

Reiter C. Constitutive insulin receptor signaling in retina and changes induced by diabetes . [Internet] [Thesis]. Penn State University; 2008. [cited 2021 Mar 03]. Available from: https://submit-etda.libraries.psu.edu/catalog/6379.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Reiter C. Constitutive insulin receptor signaling in retina and changes induced by diabetes . [Thesis]. Penn State University; 2008. Available from: https://submit-etda.libraries.psu.edu/catalog/6379

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

25. R. Rametta. UN¿AUMENTATA ESPRESSIONE DEL SUBSTRATO DEL RECETTORE DELL¿INSULINA 2 (IRS-2) È ASSOCIATA ALLA STEATOEPATITE E AL DISMETABOLISMO LIPIDICO IN PAZIENTI AFFETTI DA OBESITÀ GRAVE.

Degree: 2013, Università degli Studi di Milano

URL: http://hdl.handle.net/2434/219085

►

Design: Studio retrospettivo osservazionale. Soggetti: Abbiamo considerato 71 soggetti obesi (età compresa tra 20 e 68 anni; BMI>40 kg/m2 or BMI>35 kg/m2 in presenza di… (more)

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Design: Studio retrospettivo osservazionale. Soggetti: Abbiamo considerato 71 soggetti obesi (età compresa tra 20 e 68 anni; BMI>40 kg/m2 or BMI>35 kg/m2 in presenza di complicazioni metaboliche) classificati in tre gruppi secondo l’istologia epatica: controlli (n=12), steatosi semplice(n=27), e steatoepatite non alcolica (NASH; n=32). Abbiamo valutato i punti chiave del signalling insulinico e l’espressione genica delle molecole implicate nel pathway glucoregolatorio e nella DNL insulino dipendenti mediante PCR quantitativa real-time e Western blotting. RIASSUNTO 5 Risultati: I pazienti con steatosi semplice mostrano una ridotta fosforilazione della chinasi AKT1, responsabile della trasduzione del signalling insulinico, con conseguente sostenuta attività del fattore di trascrizione FOXO1 che media l’insulino resistenza a livello trascrizionale. Nonostante nessuna variazione significativa dell’espressione di insulin receptor substrate 1 (IRS1), i livelli proteici e di mRNA di IRS2, target di FOXO1, aumentano progressivamente con la severità della steatosi dai controlli alla NASH. L’espressione di IRS2 è correlata con la severità della steatosi, l’insulino resistenza e la dislipidemia. Nei pazienti con NASH, l’upregolazione di IRS2 è associata alla preservata attività di AKT2, che è il mediatore gli effetti stimolanti di insulina sulla DNL, e all’overespressione del suo target sterol regulatory element binding protein 1c (SREBP1c), che induce DNL a livello trascrizionale. L’overespressione sia di FOXO1 che di SREBP1c convergono sull’upregolazione della glucochinasi, che fornisce substrati alla DNL, nei pazienti con NASH. Conclusioni: La regolazione differenziale di IRS1 e IRS2 e dei loro effettori a valle AKT1 e AKT2 è coerente con l’upregolazione di FOXO1 e potrebbe giustificare lo stato paradossale di insulino resistenza a carico del pathway glucoregolatorio e l’aumentata insulino sensibilità di quello liporegolatorio tipico della steatosi e della dislipidemia in pazienti obesi con sindrome metabolica.

Abstract Increased insulin receptor substrate 2 expression is associated with steatohepatitis and altered lipid metabolism in obese subjects Objective: The aim of this study was to evaluate whether dysregulation of molecules involved in FOXO1 dependent insulin signalling in the liver is associated with de novo lipogenesis (DNL) and altered lipid metabolism in severely obese subjects. Design: Observational retrospective study. Subjects: We considered 71 obese subjects (age 20-68 years; BMI>40 kg/m2 or BMI>35 kg/m2 in the presence of metabolic complications) classified into three groups according to liver histology: normal liver (n=12), simple steatosis (n=27), and non-alcoholic steatohepatitis (NASH; n=32). Key nodes in insulin signalling and gene expression of molecules implicated in insulin dependent glucoregulatory pathway and DNL were evaluated by quantitative real-time PCR and Western blotting. Results: Patients with steatosis had decreased phosphorylation of the insulin…

Advisors/Committee Members: tutor: S.R. Fargion, coordinatore: M. Cattaneo, FARGION, SILVIA ROSSANA, CATTANEO, MARCO NATALE.

Subjects/Keywords: glucokinase; insulin receptor substrate 2 (IRS2); insulin resistance; lipogenesis; non-alcoholic fatty liver disease (NAFLD); steatosis.; Settore MED/09 - Medicina Interna

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rametta, R. (2013). UN¿AUMENTATA ESPRESSIONE DEL SUBSTRATO DEL RECETTORE DELL¿INSULINA 2 (IRS-2) È ASSOCIATA ALLA STEATOEPATITE E AL DISMETABOLISMO LIPIDICO IN PAZIENTI AFFETTI DA OBESITÀ GRAVE. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/219085

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Rametta, R.. “UN¿AUMENTATA ESPRESSIONE DEL SUBSTRATO DEL RECETTORE DELL¿INSULINA 2 (IRS-2) È ASSOCIATA ALLA STEATOEPATITE E AL DISMETABOLISMO LIPIDICO IN PAZIENTI AFFETTI DA OBESITÀ GRAVE.” 2013. Thesis, Università degli Studi di Milano. Accessed March 03, 2021. http://hdl.handle.net/2434/219085.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Rametta, R.. “UN¿AUMENTATA ESPRESSIONE DEL SUBSTRATO DEL RECETTORE DELL¿INSULINA 2 (IRS-2) È ASSOCIATA ALLA STEATOEPATITE E AL DISMETABOLISMO LIPIDICO IN PAZIENTI AFFETTI DA OBESITÀ GRAVE.” 2013. Web. 03 Mar 2021.

Vancouver:

Rametta R. UN¿AUMENTATA ESPRESSIONE DEL SUBSTRATO DEL RECETTORE DELL¿INSULINA 2 (IRS-2) È ASSOCIATA ALLA STEATOEPATITE E AL DISMETABOLISMO LIPIDICO IN PAZIENTI AFFETTI DA OBESITÀ GRAVE. [Internet] [Thesis]. Università degli Studi di Milano; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2434/219085.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Rametta R. UN¿AUMENTATA ESPRESSIONE DEL SUBSTRATO DEL RECETTORE DELL¿INSULINA 2 (IRS-2) È ASSOCIATA ALLA STEATOEPATITE E AL DISMETABOLISMO LIPIDICO IN PAZIENTI AFFETTI DA OBESITÀ GRAVE. [Thesis]. Università degli Studi di Milano; 2013. Available from: http://hdl.handle.net/2434/219085

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Univerzitet u Beogradu

26. Robajac, Dragana B., 1985-. N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima.

Degree: Hemijski fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get

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Biohemija - Biohemija proteina / Biochemistry - Biochemistry of proteins

Funkcije membranskih proteina su brojne: međućelijska komunikacija, adhezija, signalna transdukcija. Većina membranskih proteina je glikozilovana… (more)

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Biohemija - Biohemija proteina / Biochemistry - Biochemistry of proteins

Funkcije membranskih proteina su brojne: međućelijska komunikacija, adhezija, signalna transdukcija. Većina membranskih proteina je glikozilovana i N-glikani imaju važnu ulogu u formiranju trodimenzionalne strukture membranskih proteina, kao i u ispoljavanju njihove funkcije. Receptori za insulin (IR) i faktor rasta sličan insulinu tip 1 (IGF1R) su transmembranske tirozin-kinaze sa visokim stepenom homologije (u nekim domenima čak i 80%). Familija IGF receptora, pored IR i IGF1R, uključuje i receptor za faktore rasta slične insulinu tip 2 (IGF2R). Sva tri receptora (IR, IGF1R i IGF2R) su glikozilovani i obilno prisutni u placenti, gde imaju važne uloge u njenom razvoju i funkcionisanju. Placenta raste i razvija se da bi ispunila različite potrebe fetusa, pa se struktura i funkcija placente menjaju tokom gestacije. Znajući da su proteini odgovorni za biološke funkcije placente pretpostavljeno je da tokom gestacije može doći i do promene u sadržaju različitih tipova N-glikana prisutnih na membranskim proteinima. U ovoj tezi analizirani su tipovi N-glikana koji se mogu naći u sastavu membranskih glikoproteina, odnosno membranski N-glikom proteina humane placente. Ispitana je podložnost membranskog N-glikoma individualnim varijacijama i uticaju starosti majke/trudnice, kao i uticaj gestacije na membranski N-glikom. Znajući da je izmenjena glikozilacija često povezana sa izmenjenom funkcijom, kao i da izmenjena funkcija jednog ili više proteina može biti uzrok bolesti, ispitane su potencijalne promene membranskog N-glikoma u patološkim trudnoćama (kod preeklampsije) i trudnoćama komplikovanim patologijom majki (dijabetes). Uporedo je ispitan i uticaj starosti, gestacije i patologije na tip i zastupljenost različitih N-glikana koji ulaze u sastav receptora IGF sistema. Cilj je bio da se ispita da li promene na ukupnim membranskim proteinima (na N-glikomu) prate promene N-glikana prisutnih na pojedinačnim membranskim glikoproteinima važnim za rast i funkcionisanje placente...

Advisors/Committee Members: Mandić, Ljuba, 1953-.

Subjects/Keywords: membrane proteins; N-glycans; N-glycome; insulin receptor; insulin-like growth factor receptors type 1 and 2; gestational changes; aging; placenta

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Robajac, Dragana B., 1. (2016). N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Robajac, Dragana B., 1985-. “N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima.” 2016. Thesis, Univerzitet u Beogradu. Accessed March 03, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Robajac, Dragana B., 1985-. “N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima.” 2016. Web. 03 Mar 2021.

Vancouver:

Robajac, Dragana B. 1. N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Mar 03]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Robajac, Dragana B. 1. N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Georgia

27. Dhara, Animesh. Characterization of the expression, function and signaling of the ovary ecdysteroidogenic hormone in the female yellow fever mosquito, Aedes aegypti.

Degree: 2014, University of Georgia

URL: http://hdl.handle.net/10724/28506

► The neuropeptide, ovary ecdysteriodogenic hormone (OEH), is released from medial neurosecretory cells (MNCs) in the brain of female Aedes aegypti, in response to blood feeding.… (more)

▼ The neuropeptide, ovary ecdysteriodogenic hormone (OEH), is released from medial neurosecretory cells (MNCs) in the brain of female Aedes aegypti, in response to blood feeding. Transcript and protein expression profile of OEH in different body parts at different life stages and in female tissues during egg maturation cycle indicated that brain OEH is main source of OEH present in other tissues. Besides head tissue, OEH transcript was found only in ovary at any point during egg maturation cycle. The basis of OEH isolation from head extracts was its stimulation to yolk deposition in blood-fed decapitated females in vivo and ecdysteroid production by ovaries in vitro. A truncated version of OEH peptide was shown to be bioactive in a previous study. In this study, we compared the bioactivity of both full length and truncated peptides and did not see any significant difference indicating the truncated version could be the mature peptide, processed from prepropeptide. Insulin-like peptides (ILPs), in particular ILP3, are also produced by cells in the same region of the female brain and have the same demonstrated bioactivity. This study in fact showed the colocalization of OEH and ILP3 in MNCs. The functional in vivo bioassays indicated redundant functions of OEH with ILP3 in stimulating midgut digestion, nutrient storage, yolk protein synthesis and yolk uptake by the oocytes. In in vitro tissue culture condition OEH could not stimulate those functions indicating OEH required some other signals or resources to exhibit its function, shown in vivo.The study further showed, as that of ILP3, the ecdysteroidogenic function of OEH could be modulated through amino acid sensing, target of rapamycin (TOR) pathway. The signaling study revealed that despite many overlapping functions, unlike ILP3, OEH neither bound with nor activated the mosquito insulin receptor (MIR). However, OEH activated the MIR downstream protein kinase, Akt indicating that there might be some cross-talk with ILP3 signaling. As expected, OEH activated the TOR downstream signaling proteins, ribosomal S6 kinase and 4EBP1. Finally, this research demonstrated that OEH mediated activation of signaling proteins differs in a tissue specific way.

Subjects/Keywords: Ovary ecdysteroidogenic hormone (OEH); insulin-like peptides (ILPs); Aedes aegypti; egg maturation; mosquito insulin receptor (MIR); target of rapamycin (TOR)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dhara, A. (2014). Characterization of the expression, function and signaling of the ovary ecdysteroidogenic hormone in the female yellow fever mosquito, Aedes aegypti. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/28506

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dhara, Animesh. “Characterization of the expression, function and signaling of the ovary ecdysteroidogenic hormone in the female yellow fever mosquito, Aedes aegypti.” 2014. Thesis, University of Georgia. Accessed March 03, 2021. http://hdl.handle.net/10724/28506.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dhara, Animesh. “Characterization of the expression, function and signaling of the ovary ecdysteroidogenic hormone in the female yellow fever mosquito, Aedes aegypti.” 2014. Web. 03 Mar 2021.

Vancouver:

Dhara A. Characterization of the expression, function and signaling of the ovary ecdysteroidogenic hormone in the female yellow fever mosquito, Aedes aegypti. [Internet] [Thesis]. University of Georgia; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10724/28506.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dhara A. Characterization of the expression, function and signaling of the ovary ecdysteroidogenic hormone in the female yellow fever mosquito, Aedes aegypti. [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/28506

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Kentucky

28. Frazier, Hilaree N. Exploring the Role of Insulin Receptor Signaling in Hippocampal Learning and Memory, Neuronal Calcium Dysregulation, and Glucose Metabolism.

Degree: 2019, University of Kentucky

URL: https://uknowledge.uky.edu/pharmacol_etds/32

► In the late 90’s, emerging evidence revealed that the brain is insulin-sensitive, highlighted by broad expression of brain-specific insulin receptors and reports of circulating brain… (more)

Subjects/Keywords: Insulin Receptor; Hippocampus; Aging; Calcium Dysregulation; Glucose Metabolism; Brain Insulin Resistance; Behavioral Neurobiology; Cognitive Neuroscience; Molecular and Cellular Neuroscience; Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Frazier, H. N. (2019). Exploring the Role of Insulin Receptor Signaling in Hippocampal Learning and Memory, Neuronal Calcium Dysregulation, and Glucose Metabolism. (Doctoral Dissertation). University of Kentucky. Retrieved from https://uknowledge.uky.edu/pharmacol_etds/32

Chicago Manual of Style (16^th Edition):

Frazier, Hilaree N. “Exploring the Role of Insulin Receptor Signaling in Hippocampal Learning and Memory, Neuronal Calcium Dysregulation, and Glucose Metabolism.” 2019. Doctoral Dissertation, University of Kentucky. Accessed March 03, 2021. https://uknowledge.uky.edu/pharmacol_etds/32.

MLA Handbook (7^th Edition):

Frazier, Hilaree N. “Exploring the Role of Insulin Receptor Signaling in Hippocampal Learning and Memory, Neuronal Calcium Dysregulation, and Glucose Metabolism.” 2019. Web. 03 Mar 2021.

Vancouver:

Frazier HN. Exploring the Role of Insulin Receptor Signaling in Hippocampal Learning and Memory, Neuronal Calcium Dysregulation, and Glucose Metabolism. [Internet] [Doctoral dissertation]. University of Kentucky; 2019. [cited 2021 Mar 03]. Available from: https://uknowledge.uky.edu/pharmacol_etds/32.

Council of Science Editors:

Frazier HN. Exploring the Role of Insulin Receptor Signaling in Hippocampal Learning and Memory, Neuronal Calcium Dysregulation, and Glucose Metabolism. [Doctoral Dissertation]. University of Kentucky; 2019. Available from: https://uknowledge.uky.edu/pharmacol_etds/32

University of British Columbia

29. Lew, Gregory John. Studies on protein phosphorylation in response to insulin in isolated cellular fractions reconstituted with insulin receptors.

Degree: MS- MSc, Biochemistry and Molecular Biology, 1988, University of British Columbia

URL: http://hdl.handle.net/2429/27979

► The mechanism by which insulin and other polypeptide growth factors alter cellular metabolism is not fully understood. In the case of insulin, it is thought… (more)

Subjects/Keywords: Insulin – Receptors; Protein kinases; Receptor, Insulin; Protein-Tyrosine Kinases

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lew, G. J. (1988). Studies on protein phosphorylation in response to insulin in isolated cellular fractions reconstituted with insulin receptors. (Masters Thesis). University of British Columbia. Retrieved from http://hdl.handle.net/2429/27979

Chicago Manual of Style (16^th Edition):

Lew, Gregory John. “Studies on protein phosphorylation in response to insulin in isolated cellular fractions reconstituted with insulin receptors.” 1988. Masters Thesis, University of British Columbia. Accessed March 03, 2021. http://hdl.handle.net/2429/27979.

MLA Handbook (7^th Edition):

Lew, Gregory John. “Studies on protein phosphorylation in response to insulin in isolated cellular fractions reconstituted with insulin receptors.” 1988. Web. 03 Mar 2021.

Vancouver:

Lew GJ. Studies on protein phosphorylation in response to insulin in isolated cellular fractions reconstituted with insulin receptors. [Internet] [Masters thesis]. University of British Columbia; 1988. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2429/27979.

Council of Science Editors:

Lew GJ. Studies on protein phosphorylation in response to insulin in isolated cellular fractions reconstituted with insulin receptors. [Masters Thesis]. University of British Columbia; 1988. Available from: http://hdl.handle.net/2429/27979

Ohio University

30. Lesende , Vivian A. RNA Expression of Receptors for Growth Hormone, Insulin-like Growth Factor 1, and Insulin in Mouse Whole Adipose Tissue, Stromal Vascular Fraction, and Adipocytes.

Degree: MS, Biological Sciences (Arts and Sciences), 2015, Ohio University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1440105877

► Increasing rates of obesity and associated complications worldwide have increased research interest in the complex interplay of hormones, metabolism, and adiposity. There is much evidence… (more)

▼ Increasing rates of obesity and associated complications worldwide have increased research interest in the complex interplay of hormones, metabolism, and adiposity. There is much evidence indicating that hormones such as growth hormone (GH), insulin-like growth factor 1 (IGF-1), and insulin affect white adipose tissue (WAT) in a depot-specific manner. This suggests that hormone-induced intracellular signaling is more active in some WAT depots compared to others, as evidenced by hormone receptor expression levels. To add another layer of complexity, WAT is made up of many cell types with distinct functions, including adipocytes and cells of the stromal vascular fraction (SVF), which can differentially express these receptors. The purpose of this thesis is to further develop our understanding of how GH-, IGF-1-, and insulin-induced signaling affect adiposity in a WAT depot-specific manner. The original aims of this thesis were to: 1) use quantitative polymerase chain reaction (qPCR) to compare the expression of the receptors of the above hormones (GH, IGF-1, and insulin) in the SVF and adipocyte portions of the most commonly studied WAT depots in wildtype (WT) mice (subcutaneous, epididymal, retroperitoneal, and mesenteric), and 2) compare the expression of these receptors in the WAT depots of growth hormone antagonist (GHA) and WT mice. Unfortunately, due to low adipocyte RNA concentrations and purity, the first aim was adjusted to examine receptor RNA expression in whole WAT (as opposed to isolated adipocytes) and SVF. No significant differences in receptor expression were observed in the first aim, but a trend toward greater insulin receptor (IR) RNA expression in the SVF of the epididymal depot compared to the SVF of the mesenteric depot was seen. The main significant finding of the second aim was that growth hormone receptor (GHR) was more strongly expressed in GHA mice than in WT mice in the mesenteric depot, a result that could be explained by differences in SVF cell populations in GHA mesenteric WAT. Thus, future studies should focus on examining differences in WAT immune cell populations in the two genotypes, as well as optimizing the process of RNA isolation from adipocytes to allow for a more clear comparison of the two portions. Advisors/Committee Members: Berryman, Darlene (Advisor).

Subjects/Keywords: Biology; Molecular Biology; adipose tissue; stromal vascular fraction; growth hormone; insulin-like growth factor 1; insulin receptor; mouse models; adipocytes

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lesende , V. A. (2015). RNA Expression of Receptors for Growth Hormone, Insulin-like Growth Factor 1, and Insulin in Mouse Whole Adipose Tissue, Stromal Vascular Fraction, and Adipocytes. (Masters Thesis). Ohio University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1440105877

Chicago Manual of Style (16^th Edition):

Lesende , Vivian A. “RNA Expression of Receptors for Growth Hormone, Insulin-like Growth Factor 1, and Insulin in Mouse Whole Adipose Tissue, Stromal Vascular Fraction, and Adipocytes.” 2015. Masters Thesis, Ohio University. Accessed March 03, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1440105877.

MLA Handbook (7^th Edition):

Lesende , Vivian A. “RNA Expression of Receptors for Growth Hormone, Insulin-like Growth Factor 1, and Insulin in Mouse Whole Adipose Tissue, Stromal Vascular Fraction, and Adipocytes.” 2015. Web. 03 Mar 2021.

Vancouver:

Lesende VA. RNA Expression of Receptors for Growth Hormone, Insulin-like Growth Factor 1, and Insulin in Mouse Whole Adipose Tissue, Stromal Vascular Fraction, and Adipocytes. [Internet] [Masters thesis]. Ohio University; 2015. [cited 2021 Mar 03]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1440105877.

Council of Science Editors:

Lesende VA. RNA Expression of Receptors for Growth Hormone, Insulin-like Growth Factor 1, and Insulin in Mouse Whole Adipose Tissue, Stromal Vascular Fraction, and Adipocytes. [Masters Thesis]. Ohio University; 2015. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1440105877

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