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NSYSU
1.
Kuo, Yu-Fen.
POMC Overexpression Stimulates MITF/HIF-1α Survival Pathway in B16-F10 Melanoma Cells.
Degree: Master, Biological Sciences, 2008, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731 
► Melanoma is a cancer of the pigment producing cells, melanocytes, and is the most serious type of skin cancer. Cancer is a condition in which…
(more)
▼ Melanoma is a cancer of the pigment producing cells, melanocytes, and is the most serious type of skin cancer. Cancer is a condition in which one type of cell grows without limit in a disorganized fashion, disrupting and replacing normal tissues and their functions. Normal melanocytes reside in the outer layer of the skin and produce a brown pigment called melanin, which is responsible for skin color. Melanoma occurs when melanocytes become cancerous, grow, and invade other tissues. Pro-opiomelanocortin (POMC) is a precursor polypeptide of 241 amino acids and the prohormone of various neuropeptide, including corticotropin (ACTH),
α-melanocyte-stimulating hormone (α-MSH), and β-endorphin (β-EP). Recently, we demonstrated that systemic POMC overexpression potently suppresses the growth and metastasis of B16-F10 melanoma in vitro and in vivo. However, despite potent inhibition of tumor proliferation and angiogenesis, B16-F10 melanoma still managed to survive after POMC gene therapy. The underlying survival mechanism of B16-F10 melanoma remains unclear. Microphthalmia-associated transcription factor (MITF) is a basic helix-loop-helix transcription factor that plays a key role not only in melanin synthesis, but also in melanocyte development and survival. Besides, MITF binds to
the hypoxia-inducible factor-1α (HIF-1α) promoter to stimulate its transcriptional activity. In this study, we investigate the influence of POMC gene delivery on the
pro-survival MITF/HIF-1α pathway in B16-F10 melanoma cells. Quantitative RT-PCR and western blot analysis revealed that POMC gene delivery increased the MITF mRNA and protein level in B16-F10 melanoma cells. Besides, POMC gene delivery significantly enhanced the HIF-1α-driven luciferase activities in melanoma cells. By transfection and puromycin selection, we generated and characterized a MITF-knockdown B16-F10 melanoma cells (MITF KD) stably expressing short hairpin RNA against MITF. The growth, invasion, and colonies formation of MITF-KD were similar to those of vector control. However, implantation of MITF-KD cells led to melanoma with significantly reduced tumor size compared with those in mice implanted with vector control cells. Histological analysis revealed a significant reduction of CD31-positive blood vessels in implantation of MITF-KD cells-treated tumors, which was accompanied with a decrease in Ki-67-positive proliferating cells and an increase in TUNEL-positive apoptotic cells. Moreover, POMC-mediated upregulation of MITF and HIF-1 α was significantly attenuated in MITF KD-B16-F10 cells. Acetylsalicylic acid (aspirin; ASA) is widely used as an
analgesic/antipyretic drug. ASA exhibits a wide range of biological effects, including preventative effects against heart attack, stroke, and the development of some types of cancer. In our study, we found ASA enhanced cell proliferation. However, in invasion test, ASA had no effect on cell migration. POMC gene delivery elevated the mRNA and protein level of hemeoxygenase-1 (HO-1), a downstream effector of HIF-1α pathway…
Advisors/Committee Members: Hong%20Tai%22%29&pagesize-30">Ming-
Hong Tai (committee member),
Cheng, Jiin-Tsuey (chair),
REN%22%29&pagesize-30">HONG YI-REN (chair).
Subjects/Keywords: Heme oxygenase-1; Adenovirus; Proopiomelanocortin; melanoma
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APA (6th Edition):
Kuo, Y. (2008). POMC Overexpression Stimulates MITF/HIF-1α Survival Pathway in B16-F10 Melanoma Cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kuo, Yu-Fen. “POMC Overexpression Stimulates MITF/HIF-1α Survival Pathway in B16-F10 Melanoma Cells.” 2008. Thesis, NSYSU. Accessed March 05, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kuo, Yu-Fen. “POMC Overexpression Stimulates MITF/HIF-1α Survival Pathway in B16-F10 Melanoma Cells.” 2008. Web. 05 Mar 2021.
Vancouver:
Kuo Y. POMC Overexpression Stimulates MITF/HIF-1α Survival Pathway in B16-F10 Melanoma Cells. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Mar 05].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kuo Y. POMC Overexpression Stimulates MITF/HIF-1α Survival Pathway in B16-F10 Melanoma Cells. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
2.
Zeng, Jun-Yan.
New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line.
Degree: Master, Biological Sciences, 2015, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019115-165758
► Antimitotic drug, combretastatin A-4 (CA-4) is a natural plant extract exhibits powerful anticancer and anti-angiogenesis activity by targeting microtubule formation. CA-4 enediyne derivatives, such as…
(more)
▼ Antimitotic drug, combretastatin A-4 (CA-4) is a natural plant extract exhibits powerful anticancer and anti-angiogenesis activity by targeting microtubule formation. CA-4 enediyne derivatives, such as LO-OMe and LO-NH2 were shown to possess potent cytotoxicity in various cancer cell lines except human neuroblastoma cell. Here, we further investigate the cytotoxic effects of LO-OMe and LO-NH2 on neuroblastoma SH-SY5Y cells. Our viability assay demonstrated that LO-OMe and LO-NH2 mediated 50 percent killing of SH-SY5Y cells at a concentration of 3.2 and 2.1 µM, respectively. Cell lysates of drug treated cells were collected for analyzing markers of cellular autophagy and apoptosis using antibodies against LC3, p62, caspase-3, cleaved PARP. The results indicated a dose-dependent increase of LC3-II/LC3-I ratio and p62 protein upon drug treatments. In addition, consistent effects were observed in GFP-LC3 reporter H4 cell line. Both compounds elicited the increase in the number and the size of GFP-LC3 puncta, indicating an accumulation of autophagosomes in reporter cells. Our previous data showed LO-OMe and LO-NH2 treatment led to cell cycle arrest at G2/M. In addition, LO-OMe and LO-NH2 also significantly unregulated the level of active caspase-3, which resolved in the increase of cleaved-PARP. In summary, our results showed that LO-OMe and LO-NH2 induced the increase of autophagosomes. The accumulation of p62 indicated an inhibition in the fusion between autophagosome and lysosome, which might be due to the interference of microtubule polymerization exerted by these compounds. Unresolved cellular stress then resulted in programmed cell death of SH-SY5Y neuroblastoma cells. However, the molecular details awaits further investigation.
Advisors/Committee Members: Ming-Jung Wu (chair), Jiin-Tsuey Cheng (committee member), Ren%22%29&pagesize-30">
Hong Yi-
Ren (chair).
Subjects/Keywords: Combretastatin A-4; LO-OMe; LO-NH2; PARP; Caspase-3; Apoptosis; Autophagy; p62; LC3
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APA (6th Edition):
Zeng, J. (2015). New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019115-165758
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Zeng, Jun-Yan. “New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line.” 2015. Thesis, NSYSU. Accessed March 05, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019115-165758.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Zeng, Jun-Yan. “New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line.” 2015. Web. 05 Mar 2021.
Vancouver:
Zeng J. New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line. [Internet] [Thesis]. NSYSU; 2015. [cited 2021 Mar 05].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019115-165758.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Zeng J. New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line. [Thesis]. NSYSU; 2015. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019115-165758
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
3.
Wang, Yin-Hsuan.
The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells.
Degree: Master, Biological Sciences, 2017, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0404117-114837
► We previously described that PKA/GSKIP/GSK3β complex serves as a platform to anchor and phosphorylate Drp1 affecting mitochondria dynamics to provide neuroprotection. Recently, a known PKA/GSK3β…
(more)
▼ We previously described that PKA/GSKIP/GSK3β complex serves as a platform to anchor and phosphorylate Drp1 affecting mitochondria dynamics to provide neuroprotection. Recently, a known PKA/GSK3β substrate, Tau, has been revealed its S409 phosphorylation is associating with the termination of neuron cells in Alzheimer disease. In this study, we attempt to extend that Tau phosphorylation is also mediated by PKA/GSKIP/GSK3β working complex. Our data showed that GSKIP-WT overexpression in SH-SY5Y cells increased phosphorylation of Tau S409 site (not S214; S262; S396; S404; T205 and T212 sites) over that of PKA- and GSK3β binding-defective mutants (V41/L45 and L130) under forskolin challenge, indicating that both PKA and GSK3β bindings may be associated to phosphorylate Tau at S409 site. Surprisingly, treatment with foskion in GSKIP-WT-overexpressing SH-SY5Y cells were significantly increase Tau phosphorylation at S409, suggesting that only PKA kinase activity, but not GSK3β, is required in the GSKIP-mediated Tau phosphorylation. However, silencing of GSK3β resulted in a dramatic decrease in phosphorylation of Tau S409, revealing both GSKIP and GSK3β are crucial of PKA/GSKIP/GSK3β/Tau complex. Further, overexpressed kinase-dead GSK3β K85R (retains capacity to bind GSKIP) in SH-SY5Y cells, but not K85M (loss of capacity to bind GSKIP), has a higher Tau S409 phosphorylation, ensures that GSK3β acts solely as an anchor binding protein rather than its kinase activity in this signaling axis. Due to previous studies showed several different residues of Tau can be phosphorylated by PKA, we conducted In vitro kinase assay and provided two clear results: (1) As similar to early findings, PKA played a phosphorylation role on Ser409, Ser214 and Ser262 residues of Tau. (2) GSK3β provided a conformational shelter in PKA/GSKIP/GSK3β/Tau complex to harbor Tau Ser409 residue so that PKA is failed to phosphorylate Tau Ser409 residue. Furthermore, by using CRISPR/Cas9 system to produce APP WT/D678H and APP WT/WT ã APP D678H/D678H multifunctional stem cells (modified from an APP patient WT/D678H genotype), the results of analysis showed phosphorylation in Tau Ser262 and Ser214 residues and the Tau Ser409 intense phosphorylation in the brain of Alzheimerâs patients.. Coupling with previous findings of PKA suggested that the PKA/GSKIP/GSK3β/Tau complex may plays a key role on the development of Alzheimerâs disease. Taken together, our data provide compelling evidence to implicate that both GSKIP and GSK3β function as anchoring proteins to enhance cAMP/PKA/Tau axis signaling during Alzheimer pathogenesis.
Advisors/Committee Members: Cheng Jiin-Tsuey (chair), Ren%22%29&pagesize-30">
Hong Yi-
Ren (committee member),
Huang Chi-Ying (chair),
Chiou Shean-jaw (chair).
Subjects/Keywords: PKA; Tau; Alzheimer disease; Human induced pluripotent stem (iPS) cells; Aβ precursor protein (; GSK3β; GSKIP
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APA ·
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APA (6th Edition):
Wang, Y. (2017). The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0404117-114837
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Wang, Yin-Hsuan. “The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells.” 2017. Thesis, NSYSU. Accessed March 05, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0404117-114837.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Wang, Yin-Hsuan. “The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells.” 2017. Web. 05 Mar 2021.
Vancouver:
Wang Y. The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells. [Internet] [Thesis]. NSYSU; 2017. [cited 2021 Mar 05].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0404117-114837.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Wang Y. The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells. [Thesis]. NSYSU; 2017. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0404117-114837
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
4.
Lin, Yen-fu.
The Studies on Crystal Stability of Virus-like Particle from Dragon Grouper Betanodavirus.
Degree: Master, Marine Biotechnology and Resources, 2015, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0529115-094154
► Dragon grouper nervous necrosis virus (DGNNV), a betanodavirus, is the cause of viral nervous necrosis in dragon grouper (Epinephelus lanceolatus). In larvae and juveniles, mortality…
(more)
▼ Dragon grouper nervous necrosis virus (DGNNV), a betanodavirus, is the cause of viral nervous necrosis in dragon grouper (Epinephelus lanceolatus). In larvae and juveniles, mortality is up amount 100%. The capsid protein of the DGNNV form virus-like particles (VLPs) that were expressed in Escherichia coli. So far, Crystals of VLPs diffracted X-rays to ~7.5 Ã resolution (Luo and Lin, 2014). In this study, VLPs purified in phosphate buffer were cross-linked with DSS grown to crystals of higher resolution of diffracted X-rays. Among poly-His tagged VLPs and point-mutation, C338C6H can not form crystals while N25R29A mutant resulted in bigger size. VLPs for studies of DGNNV VLPs protein structure and function.
Advisors/Committee Members: Chain-Shing Lin (committee member), Min-Ying Wang (chair), Ren%22%29&pagesize-30">
Hong Yi-
Ren (chair),
Chi-Hsin Hsu (chair),
Liu, Wangta (chair).
Subjects/Keywords: virus-like particles; Dragon grouper nervous necrosis virus; crystallization; cross-linking
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APA ·
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MLA ·
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APA (6th Edition):
Lin, Y. (2015). The Studies on Crystal Stability of Virus-like Particle from Dragon Grouper Betanodavirus. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0529115-094154
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Lin, Yen-fu. “The Studies on Crystal Stability of Virus-like Particle from Dragon Grouper Betanodavirus.” 2015. Thesis, NSYSU. Accessed March 05, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0529115-094154.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Lin, Yen-fu. “The Studies on Crystal Stability of Virus-like Particle from Dragon Grouper Betanodavirus.” 2015. Web. 05 Mar 2021.
Vancouver:
Lin Y. The Studies on Crystal Stability of Virus-like Particle from Dragon Grouper Betanodavirus. [Internet] [Thesis]. NSYSU; 2015. [cited 2021 Mar 05].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0529115-094154.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Lin Y. The Studies on Crystal Stability of Virus-like Particle from Dragon Grouper Betanodavirus. [Thesis]. NSYSU; 2015. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0529115-094154
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
5.
Chen, Heng-Chi.
Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin.
Degree: Master, Biological Sciences, 2000, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0704100-014039
► Antiangiogenic tomor therapies have attracted intense interest for their broad-spectrum action, low toxicity, and in the case of direct endothelial targeting, an absence of drug…
(more)
▼ Antiangiogenic tomor therapies have attracted intense interest for their broad-spectrum action, low toxicity, and in the case of direct endothelial targeting, an absence of drug resistance. Among the growing list of antiangiogenic agents, endostatin has attracted most attention and been under the spotlight of numerous debates. Like other angiogenesis inhibitors, endostatin is also a proteolytic fragment (~20 kDa) from an extracellular protein, collagen XVIII. It potently inhibits endothelial cell proliferation and angiogenesis, but has no cytotoxic effects on cancer cells. Above all, therapy of experimental cancer with endostatin in rodents leads to tumor dormancy and does not induce resistance. However, the exact mechanism on how endostatin inhibited endothelial cells proliferation remains largely unknown. We have cloned mouse endostatin cDNA from mice liver by RT-PCR. After verification by DNA sequencing, endostatin cDNA was subcloned in to E.coli expression vector to express and generate large quantities of recombinant GST-fused endostatin (GST-endostatin). Unlike His-tagged endostatin, GST-endostatin is soluble and capable of inhibiting various endothelial cell lines including HUVEC, EA.hy926 and BAEC with IC50 ~ 20 nM. Flow cytometry analysis indicated GST-endostatin induced apoptosis in EA.hy926 cells. GST-endostatin also inhibited the cell migration of EA.hy926 cells toward chemoattractant bFGF with IC50 ~ 0.5 nM. Further more, GST-endostatin inhibited in vivo angiogenesis in chicken chorioallantoic membrane and suppressed tumor growth in mice bearing Lewis lung carcinoma cells. After functional characterization of GST-endostatin, we decided to use GST-endostatin and EA.hy926 cells as a model system to study the inhibitory mechanism of endostatin in endothelial cells. By using fura-2 fluorescence probe, GST-endostatin was shown to elevate the cytosolic calcium in dose-dependent manner from extracellular source. Chelation of extracellular Ca2+ by EGTA or inhibition of calcium channel by nifedipine abolished the cytotoxic effect endostatin, suggesting the calcium rise by endostatin play an important role in its inhibitory mechanism. Besides, endostatin also stimulated activity of a large- conductance calcium-activated potassium (Bkca) channel, further supporting endostatin initiated serial changes in ion channels activities in endothelial cells. Respiratory enzyme activities and endogenous ATP synthesis in endothelial cells were significantly inhibited by GST-endostatin treatment, indicating GST-endostatin depleted the energy source for endothelial cells. In summary, present study demonstrated GST-endostatin caused dramatic changes in electrophysiologic properties and decreased endogenous ATP synthesis in endothelial cells, which may participate in its inhibitory mechanism.
Advisors/Committee Members: Shiuan, David (chair), Cheng, Jiin-Tsuey (committee member), Ren%22%29&pagesize-30">
Hong Yi-
Ren (chair),
Hong%20Tai%22%29&pagesize-30">Ming-Hong Tai (committee member).
Subjects/Keywords: angiogenesis; endostatin
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APA ·
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MLA ·
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Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Chen, H. (2000). Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0704100-014039
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Chen, Heng-Chi. “Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin.” 2000. Thesis, NSYSU. Accessed March 05, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0704100-014039.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chen, Heng-Chi. “Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin.” 2000. Web. 05 Mar 2021.
Vancouver:
Chen H. Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin. [Internet] [Thesis]. NSYSU; 2000. [cited 2021 Mar 05].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0704100-014039.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chen H. Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin. [Thesis]. NSYSU; 2000. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0704100-014039
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
6.
Sy, Wei-Dih.
Analysis of human Dynamin IV (Dymple) gene promoter.
Degree: Master, Biological Sciences, 2003, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904103-145445
► We first identified the transcriptional regulatory element of the human dynamin IV gene (Hdyn IV; dymple). The Hdyn IV belongs to a large GTPase family.…
(more)
▼ We first identified the transcriptional regulatory element of the human dynamin IV gene (Hdyn IV; dymple). The Hdyn IV belongs to a large GTPase family. This protein has a N-terminal highly conserved tripartite GTP-binding domain, coiled-coil (CC) region, but it lacks the pleckstrin homology (PH) domain and a modestly conserved C-terminal proline rich domain (PRD).
Hdyn IV gene is enriched in subcellular membrane fractions of cytoplasmic vesicles and endoplasmic reticulum, and the function of Hdyn IV gene is considered to be associated with the functions of mitochondria. The Hdyn IV is expressed as four alternative splicing variants in all eukaryotic organisms. Our question concerning why expressions of four alternative splicing variants in brain tumor tissues?
To elucidate the regulatory mechanism and the transcription factors involved, we firstly determined the transcriptional start site by 5â RACE. We next cloned the 5â-flanking region of the Hdyn IV gene and determined the nucleotide sequence of 999 bases upstream from the transcription start site. The promoter has several potential binding sites for AP2, Sp1 binding protein, but it lacks TATA and CAAT boxes. Transfection studies using a series of Hdyn IV promoter luciferase constructs in HeLa cell demonstrate that the 5âflanking region has a promoter activity. Functional promoter element of the Hdyn IV gene was located within the â140~ +29 region. Deletion analyses demonstrated that the minimal promoter activity for the transcriptional element of Hdyn IV was detected in the sequence between nucleotides â110 and â100. Electorphoretic mobility shift assay demonstrated that a putative transcriptional factor bound to the â119 to â90 region. Site-directed mutagenesis analysis of this region revealed that nucleotides at positions â108 to â100 were essential for transactivation mediated by this element.
To summary, the data indicated that the ââCTCCCAGCAââ (-108~ -100) sequence is capable of regulating Hdyn IV gene expression. However, the protein involved in the binding of this novel sequence requires further study.
Advisors/Committee Members: Hsu, Ching-Mei (chair), Ren%22%29&pagesize-30">
Hong,
Yi-
Ren (committee member),
Cheng, Jiin-Tsuey (chair),
Cho, Chung-Lung (committee member).
Subjects/Keywords: transcription factor; promoter; DynIV
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APA ·
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MLA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Sy, W. (2003). Analysis of human Dynamin IV (Dymple) gene promoter. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904103-145445
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Sy, Wei-Dih. “Analysis of human Dynamin IV (Dymple) gene promoter.” 2003. Thesis, NSYSU. Accessed March 05, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904103-145445.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Sy, Wei-Dih. “Analysis of human Dynamin IV (Dymple) gene promoter.” 2003. Web. 05 Mar 2021.
Vancouver:
Sy W. Analysis of human Dynamin IV (Dymple) gene promoter. [Internet] [Thesis]. NSYSU; 2003. [cited 2021 Mar 05].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904103-145445.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Sy W. Analysis of human Dynamin IV (Dymple) gene promoter. [Thesis]. NSYSU; 2003. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904103-145445
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
. 
Open Access Theses and Dissertations