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Our results revealed that CKS1 is involved in normal glutamatergic synapse development and dendritic spine maturation in adult hippocampus through modulating p27 (zeige CDKN1B Proteine) stability.
Cks1 is critical for Bcr-Abl (zeige ABL1 Proteine)-induced cytokine-independent clonogenic activity.
show that CKS2 counteracts CKS1 and stabilizes p27 (zeige CDKN1B Proteine)
Cks1 is overexpressed in various B cell malignancies, is required for tumor cell proliferation but is not sufficient to induce hematopoietic malignancies.
establish p27(Kip1 (zeige CDKN1B Proteine))-independent functions of Cks1 in regulating the G(1)-S transition
Collectively, these findings suggest that Cks1 targets, in addition to p27(Kip1 (zeige CDKN1B Proteine)), are critical for Myc (zeige MYC Proteine)-driven proliferation and tumorigenesis.
FGFR (zeige FGFR2 Proteine) kinase regulates the cell cycle through phosphorylation-dependent release of Cks1 from FGFR substrate 2 (zeige FRS2 Proteine)
Elevated expression of Cks1 may contribute to prostate tumorigenesis by promoting proliferation, anchorage-independent growth and migration of the cells, and elevated expression of Cks2 by protecting cells from undergoing programmed cell death.
Data show that cyclin-dependent kinase-associated proteins Cks1 and Cks2 are essential during early embryogenesis and for cell cycle progression in somatic cells.
Multiple myeloma patients with CKS1B amplification are more likely to have additional high-risk cytogenetic abnormalities and a shorter PFS and OS after an auto-HCT.
Loss of miR (zeige MLXIP Proteine)-1258 contributes to carcinogenesis and progression of liver cancer through targeting CKS1B.
High CKS1B gene expression correlates with disease onset and progression of Multiple Myeloma and associated with more extra copies of 1q21.
we overexpressed CKS1B in multiple cell lines and found increased sensitivity to PLK1 knockdown and PLK1 drug inhibition. Finally, combined inhibition of WEE1 and PLK1 results in less apoptosis than predicted based on an additive model of the individual inhibitors, showing an epistatic interaction and confirming a prediction of the yeast data.
High expression of Cks1 was significantly associated with lymph node metastasis and survival status in nasopharyngeal carcinoma
Results show that Cks1 and Cks2 promoted proliferation and prevented apoptosis of hepatocellular carcinoma HepG2 cells.
Specifically, CKS1B and MAP2K5 (zeige MAP2K5 Proteine) significantly inhibited hepatitis C viral RNA replication. PACSIN1 (zeige PACSIN1 Proteine), by contrast, inhibited hepatitis C virus infection by decreasing the level of viral protein p7.
Regulation of Cks1 protein stability is crucially dependent on specific tyrosine and lysine residues which are potential sites for post-translational modifications.
We conclude that perturbing the Hsp90 pathway could provide a useful therapeutic strategy in tumors driven by Cks1 overexpression
Our results suggest a role for CKS1B in the multiple step process of progression of MGUS to MM and show that CKS1B copy gain has a more significant prognostic value than its overexpression.
CKS1B protein binds to the catalytic subunit of the cyclin dependent kinases and is essential for their biological function. The CKS1B mRNA is found to be expressed in different patterns through the cell cycle in HeLa cells, which reflects a specialized role for the encoded protein. At least two transcript variants have been identified for this gene, and it appears that only one of them encodes a protein.
cyclin-dependent kinases regulatory subunit 1
, CDC28 protein kinase regulatory subunit 1B
, CDC28 protein kinase regulatory subunit 1B-A
, CDC28 protein kinase regulatory subunit 1B-B
, CDC28 protein kinase 1B
, cyclin-dependent kinase regulatory subunit 1
, sid 1334
, CDC2-associated protein CKS1
, CDC28 protein kinase 1
, NB4 apoptosis/differentiation related protein
, cell division control protein CKS1
, CDC28 protein kinase regulatory subunit 1