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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 stability.
Cks1 is critical for Bcr-Abl-induced cytokine-independent clonogenic activity.
show that CKS2 counteracts CKS1 and stabilizes p27
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)-independent functions of Cks1 in regulating the G(1)-S transition
Collectively, these findings suggest that Cks1 targets, in addition to p27(Kip1), are critical for Myc-driven proliferation and tumorigenesis.
FGFR kinase regulates the cell cycle through phosphorylation-dependent release of Cks1 from FGFR substrate 2
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.
miR-204 inhibits cell proliferation in gastric cancer by targeting CKS1B, CXCL1 and GPRC5A.
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-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 significantly inhibited hepatitis C viral RNA replication. PACSIN1, 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.
EGF upregulates the mRNA and protein levels of Skp2/Cks1 and p27(kip1) via the PI3K/Akt pathway and direct binding of E2F1 transcription factor with the Skp2 promoter in extrahepatic cholangiocarcinoma cells.
CKS1 mRNA and protein expression were increased in esophageal carcinoma. Overexpression of CKS1 was associated with higher grad, regional lymph node invasion, and neoplastic embolus. CKS1 was negatively associated with the p27(kip1) level in the tumor.
We demonstrated that high expression of CKS1B immunostaining can be one potent prognostic factor for disease-specific survival, metastasis-free survival, and local recurrence-free survival in patients with nasopharyngeal carcinoma.
Anaplastic multiple myeloma was associated with significantly higher prevalence of CKS1B amplification than non-anaplastic multiple myeloma.
CKS1B analysis predicts 1q21 amplification and adverse outcome for risk stratification of patients with multiple myeloma.
cyclin kinase subunit 1B nuclear expression detected by immunohistochemistry is an adverse prognostic factor for patients with multiple myeloma treated with bortezomib therapy
Cks1 is overexpressed in esophageal squamous cell carcinoma tissues. Overexpression correlates with increased radiotherapy resistance of esophageal squamous cell carcinoma.
Overexpression of Cks1 or Cks2 in human mammary epithelial and breast cancer-derived cells, as well as in other cell types, leads to override of the intra-S-phase checkpoint.
In hepatoma cells, Cks1 controlled IL-8 expression by targeting the NF-kappaB regulator IkappaBalpha, which led to NF-kappaB activation, via a p27-independent regulation of IkappaB kinase complex components.
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