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NEUROD1 - 版本历史
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{{Infobox_gene}}<br />
'''NEUROD1'''，（[[小家鼠|小鼠]]的同源蛋白質記爲NeuroD1）在人體內是NeuroD蛋白家族下的一個[[轉錄因子]]，由''NEUROD1''基因編碼。NEUROD1在[[神經系統]]發育中扮演重要角色，於發育中參與調控多種神經系細胞的分化過程<ref>{{Cite journal|title=NeuroD1/beta2 contributes to cell-specific transcription of the proopiomelanocortin gene|url=https://journals.asm.org/doi/10.1128/MCB.17.11.6673|last=Poulin|first=G|last2=Turgeon|first2=B|date=1997-11|journal=Molecular and Cellular Biology|issue=11|doi=10.1128/MCB.17.11.6673|volume=17|pages=6673–6682|language=en|issn=0270-7306|pmc=232521|pmid=9343431|last3=Drouin|first3=J|access-date=2021-11-10|archive-date=2021-11-10|archive-url=https://web.archive.org/web/20211110142059/https://journals.asm.org/doi/10.1128/MCB.17.11.6673}}</ref><ref>{{cite web|title=NEUROD1|url=http://www.uniprot.org/uniprot/Q13562|accessdate=2018-02-25|publisher=UniProt|archive-url=https://web.archive.org/web/20180225210510/http://www.uniprot.org/uniprot/Q13562|archive-date=2018-02-25|dead-url=no}}</ref>。<br />
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證據表明NEUROD1與[[II型糖尿病]]的發生關係密切<ref name="entrez">{{Cite web|title=NEUROD1 neuronal differentiation 1 [Homo sapiens (human)] - Gene - NCBI|url=https://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=ShowDetailView&TermToSearch=4760|access-date=2021-11-10|work=www.ncbi.nlm.nih.gov|archive-date=2021-11-10|archive-url=https://web.archive.org/web/20211110142058/https://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=ShowDetailView&TermToSearch=4760}}</ref>。一項研究表明在小鼠[[大腦]]內過表達NEUROD1可使[[神經膠質細胞]]轉分化爲[[神經元]]<ref>{{Cite journal|title=In Vivo Direct Reprogramming of Reactive Glial Cells into Functional Neurons after Brain Injury and in an Alzheimer’s Disease Model|url=https://linkinghub.elsevier.com/retrieve/pii/S193459091300550X|last=Guo|first=Ziyuan|last2=Zhang|first2=Lei|date=2014-02|journal=Cell Stem Cell|issue=2|doi=10.1016/j.stem.2013.12.001|volume=14|pages=188–202|language=en|pmc=3967760|pmid=24360883|last3=Wu|first3=Zheng|last4=Chen|first4=Yuchen|last5=Wang|first5=Fan|last6=Chen|first6=Gong|access-date=2021-11-10|archive-date=2022-02-17|archive-url=https://web.archive.org/web/20220217225951/https://linkinghub.elsevier.com/retrieve/pii/S193459091300550X}}</ref>。<br />
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==蛋白质相互作用==<br />
已知NEUROD1会和[[周期蛋白D1]]<ref name="pmid11788592">{{Cite journal|title=Cyclin D1 represses the basic helix-loop-helix transcription factor, BETA2/NeuroD|url=https://pubmed.ncbi.nlm.nih.gov/11788592|last=Ratineau|first=Christelle|last2=Petry|first2=Mary W.|date=2002-03-15|journal=The Journal of Biological Chemistry|issue=11|doi=10.1074/jbc.M110747200|volume=277|pages=8847–8853|issn=0021-9258|pmid=11788592|last3=Mutoh|first3=Hiroyuki|last4=Leiter|first4=Andrew B.|access-date=2021-11-10|archive-date=2021-11-10|archive-url=https://web.archive.org/web/20211110142107/https://pubmed.ncbi.nlm.nih.gov/11788592/}}</ref>、[[MAFA (基因)|MAFA]]<ref name="pmid15665000">{{Cite journal|title=The islet beta cell-enriched MafA activator is a key regulator of insulin gene transcription|url=https://pubmed.ncbi.nlm.nih.gov/15665000|last=Zhao|first=Li|last2=Guo|first2=Min|date=2005-03-25|journal=The Journal of Biological Chemistry|issue=12|doi=10.1074/jbc.M409475200|volume=280|pages=11887–11894|issn=0021-9258|pmid=15665000|last3=Matsuoka|first3=Taka-Aki|last4=Hagman|first4=Derek K.|last5=Parazzoli|first5=Susan D.|last6=Poitout|first6=Vincent|last7=Stein|first7=Roland|access-date=2021-11-10|archive-date=2022-04-19|archive-url=https://web.archive.org/web/20220419144730/https://pubmed.ncbi.nlm.nih.gov/15665000/}}</ref>、[[MAP3K10]]<ref name="pmid12881483">{{Cite journal|title=Stimulation of NeuroD activity by huntingtin and huntingtin-associated proteins HAP1 and MLK2|url=http://www.pnas.org/cgi/doi/10.1073/pnas.1133382100|last=Marcora|first=E.|last2=Gowan|first2=K.|date=2003-08-05|journal=Proceedings of the National Academy of Sciences|issue=16|doi=10.1073/pnas.1133382100|volume=100|pages=9578–9583|language=en|issn=0027-8424|pmc=170960|pmid=12881483|last3=Lee|first3=J. E.}}</ref>发生[[蛋白質交互作用|相互作用]]。<br />
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==參考==<br />
{{reflist}}<br />
{{biochem-stub}}<br />
{{转录因子与细胞内受体|g1}}<br />
[[Category:人类蛋白质]]<br />
[[Category:神经系统胚胎学]]</div>
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