ArticleMolecular and cellular biology2001
MAT1-modulated CAK activity regulates cell cycle G(1) exit.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Strategies to generate functionally normal neutrophils to reduce infection and infection-related mortality in cancer chemotherapy.Pharmacology & therapeutics · 2019Review
- MNAT1 is overexpressed in colorectal cancer and mediates p53 ubiquitin-degradation to promote colorectal cancer malignance.Journal of experimental & clinical cancer research : CR · 2018Article
- MAT1 correlates with molecular subtypes and predicts poor survival in breast cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2018Article
- Regeneration of the lung alveolus by an evolutionarily conserved epithelial progenitor.Nature · 2018Article
- Dihydromyricetin prevents cardiotoxicity and enhances anticancer activity induced by adriamycin.Oncotarget · 2015Article
- Role of cell cycle regulatory molecules in retinoic acid- and vitamin D3-induced differentiation of acute myeloid leukaemia cells.Cell proliferation · 2014Review
- The lost intrinsic fragmentation of MAT1 protein during granulopoiesis promotes the growth and metastasis of leukemic myeloblasts.Stem cells (Dayton, Ohio) · 2013Article
- MAT2B-GIT1 interplay activates MEK1/ERK 1 and 2 to induce growth in human liver and colon cancer.Hepatology (Baltimore, Md.) · 2013Article
- Retinoid-regulated FGF8f secretion by osteoblasts bypasses retinoid stimuli to mediate granulocytic differentiation of myeloid leukemia cells.Molecular cancer therapeutics · 2012Article
- Retinoid-suppressed phosphorylation of RARalpha mediates the differentiation pathway of osteosarcoma cells.Oncogene · 2010Article
- Loss of CAK phosphorylation of RAR{alpha} mediates transcriptional control of retinoid-induced cancer cell differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Association of differentially expressed genes with activation of mouse hepatic stellate cells by high-density cDNA microarray.World journal of gastroenterology · 2004Article
- Inability to enter S phase and defective RNA polymerase II CTD phosphorylation in mice lacking Mat1.The EMBO journal · 2001Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cyclin-dependent kinase (CDK)-activating kinase (CAK) is involved in cell cycle control, transcription, and DNA repair (E. A. Nigg, Curr. Opin. Cell. Biol. 8:312-317, 1996). However, the mechanisms of how CAK is integrated into these signaling pathways remain unknown. We previously demonstrated that abrogation of MAT1 (ménage à trois 1), an assembly factor and targeting subunit of CAK, induces G(1) arrest (L. Wu, P. Chen, J. J. Hwang, L. W. Barsky, K. I. Weinberg, A. Jong, and V. A. Starnes, J. Biol. Chem. 274:5564-5572, 1999). This result led us to investigate how deregulation of CAK by MAT1 abrogation affects the cell cycle G(1) exit, a process that is regulated most closely by phosphorylation of retinoblastoma tumor suppressor protein (pRb). Using mammalian cellular models that undergo G(1) arrest evoked by antisense MAT1 abrogation, we found that deregulation of CAK inhibits pRb phosphorylation and cyclin E expression, CAK phosphorylation of pRb is MAT1 dose dependent but cyclin D1/CDK4 independent, and MAT1 interacts with pRb. These results suggest that CAK is involved in the regulation of cell cycle G(1) exit while MAT1-modulated CAK formation and CAK phosphorylation of pRb may determine the cell cycle specificity of CAK in G(1) progression.
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