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CABLES1 encodes a protein involved in regulation of the cell cycle through interactions with several cyclin-dependent kinases.
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cables1 is important for neural differentiation during embryogenesis, in a mechanism that likely involves interactions with the Cdk5 (Montrer CDK5 Anticorps)/p35 (Montrer CDK5R1 Anticorps) kinase pathway.
We have identified four potentially pathogenic missense CABLES1 variants as a novel, although infrequent, cause of Cushing's Disease in children and young adults.
miR199a-3p and P53 (Montrer TP53 Anticorps) are coupled through CABLES1 and comprise a novel negative feedback loop that likely contributes to cardiac c-kit (Montrer KIT Anticorps)(+) cell proliferation and apoptosis.
Cables1/p21 (Montrer CDKN1A Anticorps) pathway has a strong effect on the induction of cell senescence and inhibition of cell growth, and acts as a novel regulatory mechanism in which p21 (Montrer CDKN1A Anticorps) is probably one of several downstream effector molecules to mediate Cables1.
CABLES1 is a critical regulator of corticotrope proliferation that defines a pathway often inactivated in Cushing disease
the results suggest Cables1 as a novel p21 (Montrer CDKN1A Anticorps) regulator through maintaining p21 (Montrer CDKN1A Anticorps) stability and support the model that the tumor-suppressive function of Cables1 occurs at least in part through enhancing the tumor-suppressive activity of p21 (Montrer CDKN1A Anticorps).
Results illuminated a dynamic regulatory system through which activated Akt (Montrer AKT1 Anticorps) and 14-3-3 (Montrer YWHAQ Anticorps) work directly together to neutralize a potent tumor suppressor function of Cables1.
The results did not detect a significant association. It indicated that common genetic variations in CDK5 (Montrer CDK5 Anticorps) genes might not play a role in the genetic predisposition to autism.
Analysis of the RT-PCR prducts of the CABLES1 gene showed eight intragenic deletions in its mRNA transcripts; 5/8 are the result of RNA splicing.
Mechanisms of CABLES1 gene inactivation in ovarian cancer development are reported.
Loss of Cables1 enhances tumor progression in the Apc (Montrer APC Anticorps)(Min/+) mouse model and activates the Wnt (Montrer WNT2 Anticorps)/beta-catenin (Montrer CTNNB1 Anticorps) signaling pathway. Cables1 is a tumor suppressor gene on chromosome 18q in this in vivo mouse model.
Agenesis of the corpus callosum frequency in Cables1(+/TAS (Montrer MAP3K4 Anticorps)) mice was significantly lower than that in Cables1(-/TAS (Montrer MAP3K4 Anticorps)) mice, indicating that wild-type Cables1 interfered with the dominant negative effect of Cables1(TAS (Montrer MAP3K4 Anticorps)).
Data show that oocytes lacking Cables1 exhibit lower basal levels of TAp63alpha and reduced accumulation of phosphorylated TAp63alpha in response to genotoxic stress.
Cables1 null mice exhibit a significant expansion of oocyte numbers at the expense of oocyte quality throughout adulthood.
This gene encodes a protein involved in regulation of the cell cycle through interactions with several cyclin-dependent kinases. One study (PMID: 16177568) reported aberrant splicing of transcripts from this gene which results in removal of the cyclin binding domain only in human cancer cells, and reduction in gene expression was shown in colorectal cancers (PMID: 17982127).Multiple transcript variants encoding different isoforms have been found for this gene.
Cdk5 and Abl enzyme substrate 1
, CDK5 and ABL1 enzyme substrate 1
, CDK5 and ABL1 enzyme substrate 1-like
, interactor with CDK3 1
, cdk3-binding protein ik3-1
, interactor-1 with cdk3