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抗Human RAP1A 抗体:
抗Mouse (Murine) RAP1A 抗体:
抗Rat (Rattus) RAP1A 抗体:
Human Monoclonal RAP1A Primary Antibody for FACS, ELISA - ABIN969561
Severson, Lee, Capaldo, Nusrat, Parkos: Junctional adhesion molecule A interacts with Afadin and PDZ-GEF2 to activate Rap1A, regulate beta1 integrin levels, and enhance cell migration. in Molecular biology of the cell 2009
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Human Monoclonal RAP1A Primary Antibody for FACS, ELISA - ABIN969562
Dao, Dupuy, Gavet, Caron, de Gunzburg: Dynamic changes in Rap1 activity are required for cell retraction and spreading during mitosis. in Journal of cell science 2009
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Human Monoclonal RAP1A Primary Antibody for PLA, ELISA - ABIN519632
Chen, Chuang, Huang, Fang, Huang, Tsai, Su, Shiu, Leu, Chien: Overexpression of Rap-1A indicates a poor prognosis for oral cavity squamous cell carcinoma and promotes tumor cell invasion via Aurora-A modulation. in The American journal of pathology 2013
HL-60 neutrophil-like cells expressing Rap1a(G12V) or Radil have an elongated phenotype because of enhanced uropod adhesion as they attempt to migrate on fibronectin. This elongated phenotype driven by Rap1a(G12V) or Radil is reversed by Galphai1(Q204L), but not by WT Galphai1 expression, suggesting that Galphai-GTP also regulates adhesion in immune cells at the level of, or downstream of, Radil.
these data highlight a signaling pathway in which SHP-1 acts through CrkII to reshape the pattern of Rap1 activation in the immunological synapse.
Study identifies Epac2-Rap1 signaling as a novel feedback mechanism in the heart, which controls mitochondrial reactive oxygen species production.
Data show that the Epac-Rap1 signaling axis is involved in triapine resistance.
Ubc9 is an essential regulator of ADAP where it is required for TCR-induced membrane recruitment of the small GTPase Rap1 and its effector protein RapL.
These findings provide the first evidence linking Rap1A with ovarian cancer development through the ERK/p38 and Notch signaling pathways, indicating that Rap1A may be used as a novel diagnostic marker or a therapeutic target for ovarian cancer.
High RAP1 expression is associated with neuroblastoma.
Rap1 mediates the effects of increased extracellular tension in multiple ways that are capable of contributing to tumor progression when dysregulated.
Novel mutations in RASGRP2, which encodes CalDAG-GEFI, abrogate Rap1 activation, causing platelet dysfunction
Unlike Rap1B, phosphorylation in the polybasic region of Rap1A does not detectably inhibit its prenylation or its binding to SmgGDS-607.
SHANK1 and SHANK3 act as integrin activation inhibitors by sequestering active Rap1 and R-Ras via the SPN domain and thus limiting their bioavailability at the plasma membrane.
These results suggest that Rap1 activation of ERKs requires PKA phosphorylation and KSR binding.
These data suggested that HBV-infection could up-regulate the expression of miR-203a, thus down regulated the expression of Rap1a.
Studies indicate that Rap interacting proteins decide the subcellular localization of Rap, and the interaction modes with downstream Rap effectors.
A receptor type-protein tyrosine phosphatase alpha-Src family kinase-Rap1 pathway was identified as responsible for recruiting myosin IIB to the zonula adherens in epithelial cells and supporting contractile tension.
Rap1- and Rac1-GTPase activation have roles in hypoxia/reoxygenation-experienced cancer cell migration and metastasis via the expression of thymosin beta-4
These findings provide further evidence that a crucial role for miR-203 in inhibiting metastasis of PCa through the suppression of Rap1A expression.
Our findings suggest that RAP1 may be a useful biomarker for the diagnosis of ical intraepithelial neoplasia .
RAP1-mediated MEK/ERK pathway defects in Kabuki syndrome.
Rap1 knockdown attenuates prostacyclin (PC)-induced vascular endothelial cell (EC) monolayer recovery.
Rap1 increases KRIT-1 targeting to endothelial cell-cell junctions where it suppresses stress fibers and stabilizes junctional integrity.
The product of this gene belongs to the family of RAS-related proteins. These proteins share approximately 50% amino acid identity with the classical RAS proteins and have numerous structural features in common. The most striking difference between RAP proteins and RAS proteins resides in their 61st amino acid: glutamine in RAS is replaced by threonine in RAP proteins. The product of this gene counteracts the mitogenic function of RAS because it can interact with RAS GAPs and RAF in a competitive manner. Two transcript variants encoding the same protein have been identified for this gene.
, GTP-binding protein smg p21A
, RAS-related protein RAP1A
, Ras-related protein Krev-1
, ras-related protein Rap-1A
, RAP1A, member of RAS oncogene family
, GTP-binding protein SMG-P21A
, ras-related protein Krev-1
, RAS-related protein 1a
, GTP-binding protein smg-p21A