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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 (Montrer RAB1A Kits ELISA) 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 (Montrer RAB1A Kits ELISA) in breast cancer and may be a potential therapeutic target for breast cancer management
CUL7, OBSL1 and CCDC8 (Montrer CCDC8 Kits ELISA) modulate the alternative splicing of the INSR (Montrer INSR Kits ELISA)
The CUL7, OBSL1, and CCDC8 (Montrer CCDC8 Kits ELISA) proteins form a 3M complex that functions in maintaining microtubule and genome integrity and normal development.
CUL7/Fbxw8 (Montrer FBXW8 Kits ELISA) ubiquitin ligase-mediated HPK1 degradation revealed a direct link and novel role of CUL7/Fbxw8 (Montrer FBXW8 Kits ELISA) ubiquitin ligase in the MAPK (Montrer MAPK1 Kits ELISA) 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 (Montrer FAM126A Kits ELISA)/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 (Montrer AKT1 Kits ELISA) and Erk (Montrer EPHB2 Kits ELISA) phosphorylation upon insulin (Montrer INS Kits ELISA) 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 (Montrer TP53 Kits ELISA) activity relaxes the otherwise stringent regulation of cardiomyocyte cell cycle reentry in the injured adult heart.
Dimerization o Cul7 and Parc (Montrer CUL9 Kits ELISA) is not required for all Cul7 functions and mouse embryonic development.
Cul7 forms a heterodimeric complex with Cul1 (Montrer CUL1 Kits ELISA) in a manner dependent on Fbxw8 (Montrer FBXW8 Kits ELISA).
suggested a role for p193/CUL7 in the regulation of apoptosis independently of p53 (Montrer TP53 Kits ELISA) and Parc (Montrer CUL9 Kits ELISA) activity
Results demonstrate a key role for the CUL7 E3 in targeting IRS-1 (Montrer IRS1 Kits ELISA) 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.