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human homolog is a GTP-binding protein. Additionally we are shipping and and many more products for this protein.
Showing 10 out of 37 products:
Human Polyclonal RRAD Primary Antibody for WB - ABIN2786776
Chang, Zhang, Tseng, Xie, Ilany, Brüning, Sun, Zhu, Cui, Youker, Yang, Day, Kahn, Chen: Rad GTPase deficiency leads to cardiac hypertrophy. in Circulation 2007
Human Polyclonal RRAD Primary Antibody for IF, IHC - ABIN1534965
Reynet, Kahn: Rad: a member of the Ras family overexpressed in muscle of type II diabetic humans. in Science (New York, N.Y.) 1993
Data show that Ras-related associated with diabetes protein (RRAD) directly binds to the p65 (show GORASP1 Antibodies) subunit of the NF-kappa B (NF-kappaB (show NFKB1 Antibodies))complex and inhibits the nuclear translocation of p65 (show GORASP1 Antibodies), which in turn negatively regulates the NF-kappaB (show NFKB1 Antibodies) signaling
Brg1 (show SMARCA4 Antibodies) inhibits proliferation and migration of human aortic smooth muscle cells by directly up-regulating RRAD in aortic dissection.
RRAD promotes EGFR (show EGFR Antibodies)-mediated STAT3 (show STAT3 Antibodies) activation and induces temozolomide resistance of malignant glioblastoma.
RRAD expression is frequently decreased in lung cancer. Ectopic expression of RRAD greatly reduces glycolysis whereas knockdown of RRAD promotes glycolysis in lung cancer cells.
Rad suppresses the NF-Kappa-B (show NFKB1 Antibodies) mediated transcription and downstream gene activation. Rad can directly bind to RelA/p65 (show NFkBP65 Antibodies) and suppress the interaction of RelA/p65 (show NFkBP65 Antibodies) with the NF-kappa-B (show NFKB1 Antibodies) response DNA element.
Ras(V12)-mediated oncogenic transformation induces RRAD epigenetic inactivation, which in turn promotes glucose uptake and may contribute to ovarian cancer
RRAD hypermethylation is associated with esophageal squamous cell carcinoma.
Mouse Rad Q65P (the murine equivalent of human Rad Q66P) inhibits L-type currents conducted by CaV1.2 (show CACNA1C Antibodies) or CaV1.3 (show CACNA1D Antibodies) channels as potently as wild-type Rad (>95% inhibition of both channels).
Rad over expression could be a molecular target to improve bortezomib sensitivity in human leukemia and lymphoma.
results indicate that RRAD might act as a functional tumor suppressor and its epigenetic inactivation may play an important role in NPC (show NPC1 Antibodies) development
The Rad(-/-) phenotype is marked by enhanced systolic and diastolic function, which is consistent with a model that does not progress into heart failure.
Rad, Gem (show GEM Antibodies) and Rem (show REM1 Antibodies) all reduce depolarization-dependent Ca2 (show CA2 Antibodies)+ entry in developing myotubes.
A dominant-negative Rad mutation causes arrhythmogenesis via PKA-mediated phosphorylation of RYR2 (show RYR2 Antibodies) activity in the heart.
Depletion of Rad GTPase (show RACGAP1 Antibodies) increases L-type calcium channel current leading to increased cardiac contraction, without stimulating cardiac hypertrophy.
Rad GTPase (show RACGAP1 Antibodies) inhibits cardiac fibrosis through connective tissue growth factor (show CTGF Antibodies) in failing hearts.
both Rem (show REM1 Antibodies) and Rad bind directly to Ca2 (show CA2 Antibodies)+ channel beta-subunits (CaV (show CA5A Antibodies) beta) in vivo
These results demonstrate a potential synergistic interaction between increased expression of Rad and high-fat diet in creation of insulin (show INS Antibodies) resistance and altered lipid metabolism present in type 2 diabetes.
Nuclear localization of RGK proteins (Rad, Rem (show REM1 Antibodies), and Rem2 (show REM2 Antibodies)) contributes to the suppression of RGK-mediated cell shape remodeling.
Rad is a novel mediator that inhibits cardiac hypertrophy through the CaMKII (show CAMK2G Antibodies) pathway
human homolog is a GTP-binding protein
Ras-related associated with diabetes
, GTP-binding protein RAD
, RAS (RAD and GEM) like GTP binding 3
, ras associated with diabetes
, Ras-like GTP-binding protein rad