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Hepatocellular carcinoma patients with positive expression for both Rabl3 and Cullin7 had a remarkably shorter survival time compared with patients with negative expression for both proteins.
our study provided evidence that Cullin7 functions as a novel oncogene (show RAB1A ELISA Kits) in lung cancer and may be a potential therapeutic target for lung cancer management.
We report a family with variable phenotypic features of 3-M syndrome and we describe the prenatal and postnatal growth pattern of two affected sisters with a novel homozygous CUL7 mutation (c.3173-1G>C), showing a pre- and post-natal growth deficiency and a normal cranial circumference.
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 ELISA Kits) in breast cancer and may be a potential therapeutic target for breast cancer management
CUL7, OBSL1 and CCDC8 (show CCDC8 ELISA Kits) modulate the alternative splicing of the INSR (show INSR ELISA Kits)
The CUL7, OBSL1, and CCDC8 (show CCDC8 ELISA Kits) proteins form a 3M complex that functions in maintaining microtubule and genome integrity and normal development.
CUL7/Fbxw8 (show FBXW8 ELISA Kits) ubiquitin ligase-mediated HPK1 degradation revealed a direct link and novel role of CUL7/Fbxw8 (show FBXW8 ELISA Kits) ubiquitin ligase in the MAPK (show MAPK1 ELISA Kits) 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 ELISA Kits)/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.
Cul7-/- mouse embryonic fibroblasts displayed an increase in the activation of AKT (show AKT1 ELISA Kits) and Erk (show EPHB2 ELISA Kits) phosphorylation upon insulin (show INS ELISA Kits) 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 ELISA Kits) activity relaxes the otherwise stringent regulation of cardiomyocyte cell cycle reentry in the injured adult heart.
Dimerization o Cul7 and Parc (show CUL9 ELISA Kits) is not required for all Cul7 functions and mouse embryonic development.
Cul7 forms a heterodimeric complex with Cul1 (show CUL1 ELISA Kits) in a manner dependent on Fbxw8 (show FBXW8 ELISA Kits).
suggested a role for p193/CUL7 in the regulation of apoptosis independently of p53 (show TP53 ELISA Kits) and Parc (show CUL9 ELISA Kits) activity
Results demonstrate a key role for the CUL7 E3 in targeting IRS-1 (show IRS1 ELISA Kits) 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.