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Hepatitis C virus uses NS5B to specifically suppress NORE1A, facilitating viral replication and elevated Ras signaling.
Our study demonstrated that miR (show MLXIP Proteins)-214 expression was elevated and RASSF5 was down regulated in oral cancer. Moreover, miR (show MLXIP Proteins)-214 suppressed KB cell apoptosis through down regulation of RASSF5 expression
mCD40L-induced cell death mediated by NORE1A expression appeared to be independent of mCD40L-induced cell death mediated by sustained JNK (show MAPK8 Proteins) activation since NORE1A inhibition did not affect JNK (show MAPK8 Proteins) phosphorylation and vice versa
Ras induces the formation of a complex between NORE1A and the phosphatase PP1A (show PPP1CA Proteins), promoting the activation of the Rb tumor suppressor by dephosphorylation
RASSF5 expression is negatively correlated with distant metastasis of osteosarcoma, and RASSF5 may function as a tumor suppressor in OS cells through activation of the MST1/LATS1 pathway.
NORE1A allows Ras to qualitatively modify p53 (show TP53 Proteins) function to promote senescence.
NORE1A has a role in Ras regulation of SCF (show KITLG Proteins)(beta-TrCP (show BTRC Proteins)) protein activity and specificity
RASSF5 can act as an inhibitor or a potential positive regulator of Mst2 (show STK3 Proteins), depending on whether it binds to Mst2 (show STK3 Proteins) before or after activation-loop phosphorylation.
Ubiquitin ligase Itch is a unique negative regulator of RASSF5.
The RASSF gene family members RASSF5, RASSF6 (show RASSF6 Proteins) and RASSF7 show frequent DNA methylation (show HELLS Proteins) in neuroblastoma (show ARHGEF16 Proteins).
Rassf5 and Ndr1 (show STK38 Proteins) or Ndr2 (show STK38L Proteins) kinases regulate neuronal polarity through Par3 (show F2RL2 Proteins) phosphorylation.
These findings indicate that the control of HIPK1 (show HIPK1 Proteins) stability by Mdm2 (show MDM2 Proteins)-NORE1 has a major effect on cell behaviour, and epigenetic inactivation of NORE1 enables adenocarcinoma formation in vivo through HIPK1 (show HIPK1 Proteins) stabilization.
a direct role for RASSF5 in death receptor ligand-mediated apoptosis and provide further evidence for RASSF5 as a tumor suppressor.
a novel regulatory network composed of the tumor suppressor NORE1A, the mitotic kinase Aurora A, the small GTPase Ras, and the microtubule cytoskeleton.
findings define a T cell receptor "inside-out" pathway via N-SKAP1 (show SKAP1 Proteins)-C-RapL that regulates T cell adhesion, motility, and arrest times with dendritic cells in lymph nodes.
findings reveal the several critical steps of Rap1 (show TERF2IP Proteins), which are RAPL-dependent and -independent, in lymphocyte trafficking
mapping to chromosome 1 and sequence variation of the murine Ras effector gene Nore1
Nore1 is a member of a family of Ras effector/tumor suppressors that includes RASSF1 (show RASSF1 Proteins)
RAPL is a crucial immune cell trafficking regulator essential for immunosurveillance.
RAPL and Mst1 localized to vesicular compartments and dynamically translocated with LFA-1 to the leading edge upon Rap1 activation.
This gene is a member of the Ras association domain family. It functions as a tumor suppressor, and is inactivated in a variety of cancers. The encoded protein localizes to centrosomes and microtubules, and associates with the GTP-activated forms of Ras, Rap1, and several other Ras-like small GTPases. The protein regulates lymphocyte adhesion and suppresses cell growth in response to activated Rap1 or Ras. Multiple transcript variants encoding different isoforms have been found for this gene.
, Ras association (RalGDS/AF-6) domain family 5
, Ras effector-like protein
, new ras effector 1
, novel Ras effector 1
, ras association domain-containing protein 5
, regulator for cell adhesion and polarization enriched in lymphoid tissue
, tumor suppressor RASSF3
, novel ras effector 1
, regulator for cell adhesion and polarization enriched in lymphoid tissues
, protein interacting with guanine nucleotide exchange factor