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DIRAS3 is a member of the ras superfamily, and is expressed in normal ovarian and breast epithelial cells, but not in ovarian and breast cancers. Additionally we are shipping DIRAS3 Proteins (5) and many more products for this protein.
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Human Polyclonal DIRAS3 Primary Antibody for ELISA, WB - ABIN563932
Li, Ramani, Sun, Zee, Grant, Yang, Xia, Oh, Ko, Mato, Lu: Forced expression of methionine adenosyltransferase 1A in human hepatoma cells suppresses in vivo tumorigenicity in mice. in The American journal of pathology 2010
polymorphism-based approach was used to detect the imprinting status of NNAT (show NNAT Antibodies) and DIRAS3 genes in five heterozygous pigs (based on SNP) of Large White and Meishan F(1) hybrids
lncRNA GAS5 functions as a competing endogenous RNA for miR (show MLXIP Antibodies)-221 to suppress cell growth and EMT (show ITK Antibodies) in osteosarcoma by regulating the miR (show MLXIP Antibodies)-221/ARHI pathway.
DiRas3 binds to KSR1 (show KSR1 Antibodies) independently of its interaction with activated Ras and RAF (show RAF1 Antibodies).
We demonstrate that DIRAS3 knock-down (KD) in adipose stromal/progenitor cells (ASCs) induces activation of Akt (show AKT1 Antibodies)-mTOR (show FRAP1 Antibodies) signaling and proliferation arrest. DIRAS3 KD ASCs lose the potential to form colonies and are negative for Ki-67 (show MKI67 Antibodies). Moreover, silencing of DIRAS3 results in a premature senescence phenotype.
ARHI-mediated up-regulation of glycolysis and glutaminolysis was found to be autophagy-dependent and inhibition of these metabolic pathways resulted in decreased cell viability.
The overexpression of ARHI promotes colon cancer SW480 cell apoptosis by inhibiting the level of Akt (show AKT1 Antibodies).
Transcriptional, but not post-transcriptional, silencing of GNG12-AS1 (show PTGDR Antibodies) causes concomitant upregulation of DIRAS3, indicating a function in transcriptional interference.
ARHI mRNA and protein expression is markedly decreased in osteosarcoma MG-63 cells lines. Overexpression of ARHI inhibits cell viability and proliferation.
ARHI-mediated autophagy-associated cell death enhances chemosensitivity to cisplatin in ovarian cancer cell lines and xenografts.
EZH2 (show EZH2 Antibodies)-''induced H3K27me3 is associated with epigenetic repression of the ARHI tumor-suppressor gene in epithelial ovarian cancer
ARHI competes with RanGTPase and interacts with importin beta (show KPNB1 Antibodies) via basic-acidic patch interaction, which leads to inhibition of STAT3 (show STAT3 Antibodies) translocation.
This gene is a member of the ras superfamily, and is expressed in normal ovarian and breast epithelial cells, but not in ovarian and breast cancers. It is an imprinted gene, with monoallelic expression of the paternal allele, which is associated with growth suppression. Thus, this gene appears to be a putative tumor suppressor gene whose function is abrogated in ovarian and breast cancers.
DIRAS family, GTP-binding RAS-like 3
, GTP-binding protein Di-Ras3
, GTP-binding RAS-like protein 3
, distinct subgroup of the Ras family member 3
, ras homolog gene family, member I
, rho-related GTP-binding protein RhoI