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CUL4A is the ubiquitin ligase component of a multimeric complex involved in the degradation of DNA damage-response proteins (Liu et al., 2009 [PubMed 19481525]).[supplied by OMIM, Oct 2009].. Additionally we are shipping Cullin 4A Antibodies (77) and Cullin 4A Proteins (5) and many more products for this protein.
Results show that cul4a but not cul4b (show CUL4B ELISA Kits) is required for the expression of tbx5a, an essential transcription factor in heart and limb development.
Elevated expression of CUL4A is positively correlated with distant metastases.
Increased CUL4A expression is associated with osteosarcoma.
Findings indicate the importance of a microRNAs miR (show MLXIP ELISA Kits)-9/137-CUL4A-Hippo signaling axis in gastric cancer (GC), and suggest new therapeutic targets for future treatment of GC.
CUL4A facilitates hepatocarcinogenesis by promoting cell cycle progression and epithelial-mesenchymal transition.
this study proposes that inflammation-induced Jak-STAT3 signaling leads to colon cancer development through proteasomal degradation of DICER1 by ubiquitin ligase complex of CUL4A(DCAF1), which suggests a novel therapeutic opportunity for colon cancer
We observed that knockdown of Cul4A was associated with increased sensitivity to gemcitabine through upregulation of TGFBI (show TGFBI ELISA Kits) in lung cancer cells.
Amplification of CUL4A, IRS2 (show IRS2 ELISA Kits), and TFDP1 (show TFDP1 ELISA Kits) genes showed a significant difference in disease-free survival by both univariate and multivariate survival analyses in intrahepatic cholangiocarcinoma.
These results suggest a linkage between Cul4A and Gli1 (show GLI1 ELISA Kits) expression in human mesothelioma.
Our results indicate that CUL4A overexpression play an oncogenic role in the pathogenesis of prostate cancer (PC), and CUL4A may be a potential therapeutic target for PCa (show FLVCR1 ELISA Kits).
Our data are consistent with the idea that the CUL4A/B-DDB1 (show DDB1 ELISA Kits)-CRBN (show CRBN ELISA Kits) complex catalyses the polyubiquitination and thus controls the degradation of CLC-1 (show CLCN1 ELISA Kits) channels.
These studies identify CUL4-DDB1 (show DDB1 ELISA Kits) complex as a novel post-translational regulator of stem and progenitor maintenance and differentiation.
Findings indicate that Cul4A is oncogenic in vivo and that Cul4A over-expression is associated with cisplatin resistance in lung cancer cells.
this study revealed an indispensable role for Cul4a during male germ cell meiosis.
The primary spermatocytes in Cul4A-/- mice are deficient in progression through late prophase I, a time point when expression of the X-linked Cul4B (show CUL4B ELISA Kits) gene is silenced due to meiotic sex chromosome inactivation.
CUL-4A is critical for early embryonic development. CUL-4A(-/-) embryos die between 4.5 and 7.5 dpc.
Enforced CUL-4A expression does not alter the cell cycle distribution of uninduced cells. It increases the proportion of induced cells in S-phase & reduces the proportion in G0/G1. This CUL-4A regulatory function is interconnected with differentiation.
a Cul4A ubiquitin ligase (show RNF123 ELISA Kits) positively regulates proliferation by targeting p27 (show CDKN1B ELISA Kits) for degradation and that Cul4A down-regulation during terminal erythroid differentiation allows p27 (show CDKN1B ELISA Kits) to accumulate and signal cell cycle exit
Cul4A(+/-) hematopoietic stem-cells exhibit defects in engraftment and self-renewal capacity
Cul4A deficiency resulted in DNA damage and apoptosis of rapidly dividing cells, and mutant mice died within 3 to 10 days after induction with dramatic atrophy of the intestinal villi, bone marrow, and spleen, and with hematopoietic failure
CUL4A is the ubiquitin ligase component of a multimeric complex involved in the degradation of DNA damage-response proteins (Liu et al., 2009