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You searched for +publisher:"Harvard University" +contributor:("Ma, Qiufu"). Showing records 1 – 3 of 3 total matches.

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Harvard University

1. Sprague, Jared Michael. TRPV1 Sensitization in Primary Sensory Neurons.

Degree: PhD, Biological Sciences in Dental Medicine, 2014, Harvard University

Pain is a major personal and community burden throughout the world with currently limited treatment options for persistent pain due to unacceptable side effects, dependence or frank inefficacy. It is necessary to understand the anatomical and molecular pathways leading to pain to better cope with the current challenge of treating it. Advisors/Committee Members: Woolf, Clifford (advisor), Ma, Qiufu (committee member), Gaudet, Rachelle (committee member), Yellen, Gary (committee member).

Subjects/Keywords: Neurosciences; Bortezomib; Optovin; Sensitization; TRPA1; TRPV1

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

APA (6th Edition):

Sprague, J. M. (2014). TRPV1 Sensitization in Primary Sensory Neurons. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:12274115

Chicago Manual of Style (16th Edition):

Sprague, Jared Michael. “TRPV1 Sensitization in Primary Sensory Neurons.” 2014. Doctoral Dissertation, Harvard University. Accessed October 18, 2017. http://nrs.harvard.edu/urn-3:HUL.InstRepos:12274115.

MLA Handbook (7th Edition):

Sprague, Jared Michael. “TRPV1 Sensitization in Primary Sensory Neurons.” 2014. Web. 18 Oct 2017.

Vancouver:

Sprague JM. TRPV1 Sensitization in Primary Sensory Neurons. [Internet] [Doctoral dissertation]. Harvard University; 2014. [cited 2017 Oct 18]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:12274115.

Council of Science Editors:

Sprague JM. TRPV1 Sensitization in Primary Sensory Neurons. [Doctoral Dissertation]. Harvard University; 2014. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:12274115

2. Zhang, Chi. The X-linked Intellectual Disability Protein PHF6 Associates with the PAF1 Complex and Regulates Neuronal Migration in the Mammalian Brain.

Degree: PhD, Biological Sciences in Dental Medicine, 2013, Harvard University

Intellectual disability is a prevalent developmental disorder for which no effective treatments are available. Mutations of the X-linked protein PHF6 cause the Börjeson-Forssman-Lehmann syndrome (BFLS) that is characterized by intellectual disability and epilepsy. However, the biological role of PHF6 relevant to BFLS pathogenesis has remained unknown. Here, I present my dissertation research demonstrating that knockdown of PHF6 profoundly impairs neuronal migration in the mouse cerebral cortex in vivo, leading to the formation of white matter heterotopias that harbor aberrant patterns of neuronal activity. Importantly, BFLS patient specific mutation of PHF6 blocks its ability to promote neuronal migration. I also elucidate the mechanism by which PHF6 drives neuronal migration in the cerebral cortex. PHF6 physically associates with the PAF1 transcription elongation complex, and inhibition of PAF1 phenocopies the PHF6 knockdown-induced migration phenotype in vivo. I further identify Neuroglycan C (NGC), a susceptibility gene for schizophrenia, as a critical downstream target of PHF6 and the PAF1 complex, and I demonstrate that NGC mediates PHF6-dependent neuronal migration. These findings define PHF6, the PAF1 transcription elongation complex, and NGC as components of a novel cell-intrinsic transcriptional pathway that orchestrates neuronal migration in the brain, with important implications for the pathogenesis of intellectual disability and potentially other neuropsychiatric disorders. Advisors/Committee Members: Bonni, Azad (advisor), He, Xi (committee member), Arlotta, Paola (committee member), Ma, Qiufu (committee member), Lin, Yingxi (committee member).

Subjects/Keywords: Molecular biology; Neurosciences; Börjeson-Forssman-Lehman syndrome; Neuronal Migration; PAF1; PHF6; X-linked Intellectual Disability

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

APA (6th Edition):

Zhang, C. (2013). The X-linked Intellectual Disability Protein PHF6 Associates with the PAF1 Complex and Regulates Neuronal Migration in the Mammalian Brain. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:11156785

Chicago Manual of Style (16th Edition):

Zhang, Chi. “The X-linked Intellectual Disability Protein PHF6 Associates with the PAF1 Complex and Regulates Neuronal Migration in the Mammalian Brain.” 2013. Doctoral Dissertation, Harvard University. Accessed October 18, 2017. http://nrs.harvard.edu/urn-3:HUL.InstRepos:11156785.

MLA Handbook (7th Edition):

Zhang, Chi. “The X-linked Intellectual Disability Protein PHF6 Associates with the PAF1 Complex and Regulates Neuronal Migration in the Mammalian Brain.” 2013. Web. 18 Oct 2017.

Vancouver:

Zhang C. The X-linked Intellectual Disability Protein PHF6 Associates with the PAF1 Complex and Regulates Neuronal Migration in the Mammalian Brain. [Internet] [Doctoral dissertation]. Harvard University; 2013. [cited 2017 Oct 18]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11156785.

Council of Science Editors:

Zhang C. The X-linked Intellectual Disability Protein PHF6 Associates with the PAF1 Complex and Regulates Neuronal Migration in the Mammalian Brain. [Doctoral Dissertation]. Harvard University; 2013. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11156785

3. Lou, Shan. DEVELOPMENT AND FUNCTIONS OF C-LOW-THRESHOLD MECHANORECEPTORS.

Degree: PhD, Biology: Medical Sciences, Division of, 2013, Harvard University

Somatosensory neurons are essential for detecting diverse environmental stimuli, thus critical for survival of mammals. In order to achieve sensory modality specificity, many somatosensory subtypes emerge with various receptor and ion channel expression, as well as terminal morphologies. How the somatosensory system achieves such a high variety of neuronal subtypes is unknown. In this thesis, I used a newly discovered subtype, VGLUT3-expressing unmyelinated low-threshold mechanoreceptors (C-LTMRs), as a model to try to answer this question. C-LTMRs have been proposed to play a role in pleasant touch in humans or pain in mice. Previously, our lab has identified the Runt domain transcriptional factor Runx1 to be pivotal for the development of a cohort of sensory neurons such as pain related nociceptors, thermal receptors, as well as itch related pruriceptors. Here I found that Runx1 is also required to establish all known features associated with C-LTMRs. In search of the mechanism of how Runx1 controls C-LTMR development, I found that the zinc finger protein Zfp521 is predominantly expressed in C-LTMRs and its expression is Runx1 dependent. By generating and analyzing Zfp521 conditional knock out animals, I found Zfp521 is required for part of C-LTMR molecular identities and nerve terminal morphologies. Our studies suggest that Runx1 acts through Zfp521-dependent and Zfp521-independent pathways to specify C-LTMR identities. To study C-LTMR functions, we performed a series of behavioral analysis and found the loss of VGLUT3 and mechanosensitivities in C-LTMRs does not markedly affect acute or chronic mechanical pain measured from the hind paws, which argues against the proposed role of VGLUT3 in C-LTMRs in mediating mechanical pain in mice. In the future, we will continue to use our mutant mice to study physiological functions of C-LTMRs. Advisors/Committee Members: Ma, Qiufu (advisor), Segal, Rosalind (committee member), Dong, Xinzhong (committee member), Gu, Chenghua (committee member), Bean, Bruce (committee member), Macklis, Jeffery (committee member), Woolf, Clifford (committee member).

Subjects/Keywords: Neurosciences; Developmental biology; Genetics; Mechanoreceptor; Piezo2; Runx1; Somatosensory; VGLUT3; Zfp521

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

APA (6th Edition):

Lou, S. (2013). DEVELOPMENT AND FUNCTIONS OF C-LOW-THRESHOLD MECHANORECEPTORS. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:11156790

Chicago Manual of Style (16th Edition):

Lou, Shan. “DEVELOPMENT AND FUNCTIONS OF C-LOW-THRESHOLD MECHANORECEPTORS.” 2013. Doctoral Dissertation, Harvard University. Accessed October 18, 2017. http://nrs.harvard.edu/urn-3:HUL.InstRepos:11156790.

MLA Handbook (7th Edition):

Lou, Shan. “DEVELOPMENT AND FUNCTIONS OF C-LOW-THRESHOLD MECHANORECEPTORS.” 2013. Web. 18 Oct 2017.

Vancouver:

Lou S. DEVELOPMENT AND FUNCTIONS OF C-LOW-THRESHOLD MECHANORECEPTORS. [Internet] [Doctoral dissertation]. Harvard University; 2013. [cited 2017 Oct 18]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11156790.

Council of Science Editors:

Lou S. DEVELOPMENT AND FUNCTIONS OF C-LOW-THRESHOLD MECHANORECEPTORS. [Doctoral Dissertation]. Harvard University; 2013. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11156790

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