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anti-Human RAP1A Antibodies:
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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
Show all 2 Pubmed References
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
MiR-337-3p was discovered to be decreased in cervical cancer, and miR-337-3p up-regulation may inhibit the proliferation, migration and invasion and promote the apoptosis of cervical cancer cells via down-regulating Rap1A.
RRSP is a critical virulence factor that robustly inactivates Ras and Rap1 and augments the pathogenicity of invading bacteria via the combined effects of its N and C lobes.
results indicate that CD38 promotes RasGRP2/Rap1-mediated CLL cell adhesion and migration by increasing intracellular Ca2+ levels.
Microarray analysis revealed RAP1A promoted CRC growth partly through phosphatase and tensin homolog (PTEN)/forkhead box O3(FOXO3)/cyclin D1(CCND1) signaling pathway. FOXO3 overexpression could partly mimic the inhibitory effect of RAP1A knockdown in CRC growth.
Simultaneous phosphorylation of synGAP by Plk2 and CDK5 at distinct sites produces an additive increase in GAP activity toward HRas ( approximately 230%) and a smaller, non-additive increase in activity toward Rap1.
modulation of Rap1 by Pde6delta accommodates key mechanisms underlying neuronal activity
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.
the Rap1-talin 1 F0 interaction has little effect on platelet GPIIb-IIIa activation and hemostasis and cannot account for the dramatic effects of loss of Rap1 activity on these platelet functions.
Combined deficiency of RAP1A and RAP1B markedly impaired platelet aggregation, spreading, and clot retraction.
findings suggest that direct Rap1/Talin1 interaction is of particular importance in regulating the activity of different integrin classes expressed on platelets and neutrophils, which both depend on fast and dynamic integrin-mediated responses.
Rap1 plays an unanticipated role in regulating the fate of nitric oxide.
Endothelial Rap1A promotes vessel barrier maintenance in lungs in vivo, and is required for maintenance of adherens junction organization in vitro
Current results suggest an important role of basal Rap1 activation status of HSPC in their maintenance in BM for sustaining long-term adult hematopoiesis.
Data found that Rap1-/- female mice were more susceptible to DEN-induced hepatocellular carcinoma (HCC) than wild-type controls as indicated by earlier onset and increased number of both pre-neoplastic lesions and HCC, which was accompanied by a significantly decreased lifespan as the consequence of liver cancer.
Using an RNA-mediated interference screen, we identified phospholipase Cepsilon 1 (PLCepsilon1) as a crucial regulator of stromal cell-derived factor 1 alpha (SDF-1alpha)-induced Rap1 activation. We have shown that SDF-1alpha-induced activation of Rap1 is transient in comparison with the sustained level following cross-linking of the antigen receptor.
loss of Rap1 GTPases prevents the formation of axons and leading processes and thereby interferes with radial migration
neuronal Rap1 critically regulates leptin sensitivity
the Rap1-cofilin-1 pathway coordinates actin and microtubule organization at the immune synapse.
Results from comparative proteomics identified Rap1 as a novel legionella-containing-vacuole host component implicated in intracellular replication of Legionella pneumophila.
the interaction between nephrin and MAGI-1 regulates Rap1 activation in podocytes to maintain long term slit diaphragm structure
These findings ascribe a new function to SLAT, and identify Rap1 as a target of SLAT function in TCR-mediated inside-out signaling.
Rap1 Is Essential for Mouse Development and Formation of Functional Vasculature
Rap1 deficiency impaired T-cell homeostasis.
Rap1 promotes endothelial mechanosensing complex formation, NO release and normal endothelial function
RAP1-mediated MEK/ERK pathway defects in Kabuki syndrome.
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