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The protein encoded by CUL7 is a component of an E3 ubiquitin-protein ligase complex. Additionally we are shipping Cullin 7 Kits (9) and and many more products for this protein.
Showing 10 out of 52 products:
Human Polyclonal Cullin 7 Primary Antibody for EIA, IHC (p) - ABIN117952
Chen, Ma, Gao, Wang, Zhao, Wu, Wang, Xie, OuYang, Luo, Guo, Han, Liu, Wang: The active ingredients of Jiang-Zhi-Ning: study of the Nelumbo nucifera alkaloids and their main bioactive metabolites. in Molecules (Basel, Switzerland) 2012
Show all 4 references for ABIN117952
Human Polyclonal Cullin 7 Primary Antibody for ELISA, IHC - ABIN4300970
Arai, Kasper, Skaar, Ali, Takahashi, DeCaprio: Targeted disruption of p185/Cul7 gene results in abnormal vascular morphogenesis. in Proceedings of the National Academy of Sciences of the United States of America 2003
Show all 2 references for ABIN4300970
Human Polyclonal Cullin 7 Primary Antibody for IP - ABIN152033
Nelson, Glenn, Zhang, Wen, Knutson, Gouvion, Robinson, Zhou, Yang, Smith, Paulson: Selective cochlear degeneration in mice lacking the F-box protein, Fbx2, a glycoprotein-specific ubiquitin ligase subunit. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2007
report an adult female with 3-M syndrome that was caused by novel compound heterozygous mutations (c.4023-1 G>A in splice acceptor site of exon 22 and c.4359_4363dupGGCTG in exon 23) in the CUL7 gene
study provided evidence that Cullin7 functions as a novel oncogene (show RAB1A Antibodies) in breast cancer and may be a potential therapeutic target for breast cancer management
CUL7, OBSL1 and CCDC8 (show CCDC8 Antibodies) modulate the alternative splicing of the INSR (show INSR Antibodies)
The CUL7, OBSL1, and CCDC8 (show CCDC8 Antibodies) proteins form a 3M complex that functions in maintaining microtubule and genome integrity and normal development.
CUL7/Fbxw8 (show FBXW8 Antibodies) ubiquitin ligase-mediated HPK1 (show MAP4K1 Antibodies) degradation revealed a direct link and novel role of CUL7/Fbxw8 (show FBXW8 Antibodies) ubiquitin ligase in the MAPK (show MAPK1 Antibodies) pathway, which plays a critical role in cell proliferation and differentiation.
Homozygous deletion in exon 18 of the CUL7 gene, which has not been previously described, could be responsible for the 3-M syndrome.
This study demonstrates specific genomic alterations in HCC (show FAM126A Antibodies)/MS and points to CUL7 as a novel gene potentially involved in liver carcinogenesis associated with metabolic Syndrome, the amplification of which might influence cell proliferation.
Dysregulation of Cul7 and Fbxw8 (show FBXW8 Antibodies) expression might affect trophoblast turnover in intrauterine growth restriction.
Mutations in CUL7, OBSL1 and CCDC8 (show CCDC8 Antibodies) in 3-M syndrome lead to disordered growth factor signalling.
Growth factor-stimulated TBC1D3 (show TBC1D3 Antibodies) ubiquitination and degradation are regulated by its interaction with CUL7-Fbw8 (show FBXW8 Antibodies).
Cul7-/- mouse embryonic fibroblasts displayed an increase in the activation of AKT (show AKT1 Antibodies) and Erk (show EPHB2 Antibodies) phosphorylation upon insulin (show INS Antibodies) stimulation.
role of binding of Cul7 to simian virus 40 large T antigen in cell transformation; may also regulate an important growth control pathway
Antagonization of p193 and p53 (show TP53 Antibodies) activity relaxes the otherwise stringent regulation of cardiomyocyte cell cycle reentry in the injured adult heart.
Dimerization o Cul7 and Parc (show CUL9 Antibodies) is not required for all Cul7 functions and mouse embryonic development.
Cul7 forms a heterodimeric complex with Cul1 (show CUL1 Antibodies) in a manner dependent on Fbxw8 (show FBXW8 Antibodies).
suggested a role for p193/CUL7 in the regulation of apoptosis independently of p53 (show TP53 Antibodies) and Parc (show CUL9 Antibodies) activity
Results demonstrate a key role for the CUL7 E3 in targeting IRS-1 (show IRS1 Antibodies) for degradation, a process that may contribute to the regulation of cellular senescence.
Expression of the dominant interfering p193 transgene results in a decrease in infarct scar expansion and preservation of myocardial function at 4 weeks after Myocardial Infarction.
The protein encoded by this gene is a component of an E3 ubiquitin-protein ligase complex. The encoded protein interacts with TP53, CUL9, and FBXW8 proteins. Defects in this gene are a cause of 3M syndrome type 1 (3M1). Two transcript variants encoding different isoforms have been found for this gene.