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  • proliferation
  • Cdk6 expression increased myeloid progenitor proliferation, and inhibited myeloid lineageā€specific gene expression and terminal differentiation in vitro and in vivo . (embopress.org)
  • Using the OP9-DL1 system to deliver temporally controlled Notch receptor-dependent signaling, we show that CDK6 is required for Notch-dependent survival, proliferation, and differentiation. (aacrjournals.org)
  • hematopoietic
  • Since Runx transcription factors play central roles in hematopoietic, neuronal and osteogenic lineages, this novel, noncanonical Cdk6 function may control terminal differentiation in multiple tissues and cell types. (embopress.org)
  • proteins
  • The kinase CDK6 was expressed as different fusion proteins using the baculovirus expression vector system in high yields and afterwards purified. (tum.de)
  • Recombinant full-length human CDK6 and CyclinD3 were co-expressed by baculovirus in Sf9 insect cells using an N-terminal His tag on both proteins. (fishersci.com)
  • increases
  • Gu M , Lynch J and Brecher P. Nitric oxide increases p21 Waf1/Cip1 expression by a cGMP-dependent pathway that includes activation of extracellular signal-regulated kinase and p70S6K. (tuftsmedicalcenter.org)
  • Requirement
  • These results show a critical requirement for CDK6 in Notch/Akt-dependent T-cell development and tumorigenesis and strongly support CDK6 as a specific therapeutic target in human lymphoid malignancies. (aacrjournals.org)
  • role
  • To determine the role of CDK6 in development and tumorigenesis, we generated and analyzed knockout mice. (aacrjournals.org)
  • Consistent with a key role for CDK6 as a D-cyclin partner in thymocytes, knockout (KO) of CDK4 or CDK2 was shown to have no significant effect on T-cell development ( 11 , 12 ), but significantly decreased thymic cellularity was observed in a CDK6 KO animal ( 13 ). (aacrjournals.org)
  • 15 - 18 ) suggest a role for CDK6 in T-cell malignancies. (aacrjournals.org)
  • However, the specific role of CDK6 in thymocyte development is unclear and the effect of CDK6 loss on T-cell tumorigenesis has not been ascertained. (aacrjournals.org)
  • target
  • Furthermore, CDK6-deficient mice were resistant to lymphomagenesis induced by active Akt, a downstream target of Notch signaling. (aacrjournals.org)
  • We report that CDK6 acts as a downstream target of Notch and Akt and is essential for T-cell development and tumorigenesis. (aacrjournals.org)