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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].. De plus, nous expédions Cullin 4A Protéines (4) et et beaucoup plus de produits pour cette protéine.
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Human Polyclonal Cullin 4A Primary Antibody pour IP, WB - ABIN233773
Leung-Pineda, Huh, Piwnica-Worms: DDB1 targets Chk1 to the Cul4 E3 ligase complex in normal cycling cells and in cells experiencing replication stress. dans Cancer research 2009
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Human Polyclonal Cullin 4A Primary Antibody pour IP - ABIN250652
Vaites, Lee, Lian, Barbash, Roy, Wasik, Klein-Szanto, Rustgi, Diehl: The Fbx4 tumor suppressor regulates cyclin D1 accumulation and prevents neoplastic transformation. dans Molecular and cellular biology 2011
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Human Polyclonal Cullin 4A Primary Antibody pour ICC, IF - ABIN250653
Jiang, Rong, Sheikh, Huang: Cullin-4A·DNA damage-binding protein 1 E3 ligase complex targets tumor suppressor RASSF1A for degradation during mitosis. dans The Journal of biological chemistry 2011
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Human Polyclonal Cullin 4A Primary Antibody pour ELISA, IHC - ABIN4300968
Higa, Mihaylov, Banks, Zheng, Zhang: Radiation-mediated proteolysis of CDT1 by CUL4-ROC1 and CSN complexes constitutes a new checkpoint. dans Nature cell biology 2003
Results show that cul4a but not cul4b (Montrer CUL4B Anticorps) is required for the expression of tbx5a, an essential transcription factor in heart and limb development.
The identification of CUL4A as a downstream target of TGF-beta1 (Montrer TGFB1 Anticorps) represents a critical pro-survival mechanism in breast cancer progression and provides another point for therapeutic intervention in breast cancer.
Our data demonstrate that overexpression of CUL4A plays an oncogenic role in iCCA (Montrer PRRT2 Anticorps) and adversely affects disease-free survival. Thus, it may prove to be a powerful prognostic factor and a potential therapeutic target.
JMJD2C (Montrer KDM4C Anticorps) regulated the activities of lung cancer cells by directly controlling the expression of CUL4A in JMJD2C (Montrer KDM4C Anticorps) over-expression cell line.
plays a critical role in perihilar cholangiocarcinoma (PHCC) metastasis by facilitating PHCC cell motility and cell invasion as well as consequent induction of epithelial to mesenchymal transition via, at least partially, up-regulating transcriptional regulation factor ZEB1 (Montrer ZEB1 Anticorps)
The CUL4A interacts with WD-40 proteins through the adaptor protein DNA damage-binding protein 1 (DDB1) to target substrates for ubiquitylation.
knockdown of cullin 4A via small interfering RNA inhibited the proliferation of the multiple myeloma cell lines by delaying cell-cycle progression and increasing apoptosis. cullin 4A downregulation inhibited multiple myeloma cell migration and invasion in vitro. Our results suggested that cullin 4A could be a promising therapy target in multiple myeloma patients
findings revealed that CUL4A and CUL4B (Montrer CUL4B Anticorps) are differentially associated with etiologic factors for pulmonary malignancies and are independent prognostic markers for the survival of distinct lung cancer subtypes
decreased tumour growth and increased chemosensitivity to gemcitabine were also noted after Cul4A knockdown.
CUL4A played an oncogene (Montrer RAB1A Anticorps) role through ZEB1 (Montrer ZEB1 Anticorps) in IL-6 (Montrer IL6 Anticorps)-induced colorectal carcinoma progression.
Overexpression of miR (Montrer MLXIP Anticorps)-494 inhibited proliferation, migration, invasion and EMT (Montrer ITK Anticorps) of ovarian cancer cells by directly suppressing CUL4A expression. Therefore, our findings indicate that miR (Montrer MLXIP Anticorps)-494/CUL4A axis is important in the control of ovarian cancer tumorigenesis.
These studies identify CUL4-DDB1 complex as a novel post-translational regulator of stem and progenitor maintenance and differentiation.
CUL4A facilitates hepatocarcinogenesis by promoting cell cycle progression and epithelial-mesenchymal transition.
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 (Montrer CUL4B Anticorps) 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 (Montrer RNF123 Anticorps) positively regulates proliferation by targeting p27 (Montrer CDKN1B Anticorps) for degradation and that Cul4A down-regulation during terminal erythroid differentiation allows p27 (Montrer CDKN1B Anticorps) 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