Molecular Control of Atypical Protein Kinase C: Tipping the Balance between Self-Renewal and Differentiation
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- 作者：Michael L. Drummond ; Kenneth E. Prehoda ; prehoda@uoregon.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：PKC ; protein kinase C ; aPKC ; atypical protein kinase C ; PrE ; primitive endoderm ; NB ; neuroblast ; Par ; partitioning defective ; Pros ; Prospero ; Brat ; brain tumor ; GMC ; ganglion mother cell ; Cdk2 ; cyclin-dependent kinase 2 ; HH ; hedgehog ; Ptch ; patched ; Smo ; smoothened ; BCC ; basal cell carcinomas ; LSCC ; lung squamous cell carcinoma ; HHAT ; HH acyl transferase ; JAK ; Janus kinase ; Stat ; Signal transducer and activator of transcription
- 刊名：Journal of Molecular Biology
- 出版年：2016
- 出版时间：10 April 2016
- 年：2016
- 卷：428
- 期：7
- 页码：1455-1464
- 全文大小：1004 K
文摘
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atypical Protein Kinase C (aPKC) regulates stem cell fate decision using multiple mechanisms.
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aPKC polarizes fate determinant proteins during asymmetric cell division.
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aPKC shortens the cell cycle to promote cell proliferation.
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aPKC phosphorylates conserved transcription factors to regulate cell fate decisions.
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aPKC controls cell fate decision by polarity dependent and independent mechanisms.