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We solved the crystal structure of IN-RA-PH to a resolution of 2.4-A. The structure reveals that the IN segment associates with the RA segment and thereby suppresses RIAM:RAP1 association. This autoinhibitory configuration of RIAM can be released by phosphorylation at Tyr45 in the IN segment.
Findings identified eyes absent homolog 4 (EYA4) as a tumor suppressor that disrupts aberrant activation of the nuclear factor kappa B (NF-kappaB)/RAP1 protein signaling pathway and thus orchestrates a physiological impediment to hepatocellular carcinoma (HCC) growth and invasion.
These data reveal a MAPK pathway-independent switch in response to cAMP signaling during melanoma progression.Implications: The prosurvival mechanism involving the cAMP-EPAC-RAP1 signaling pathway suggest the potential for new targeted therapies in melanoma.
Rap1 telomeric and non-telomeric functions and potential implications in diabetic cardiomyopathy have been discussed. (Review)
the cytoplasmic RAP1-NF-kappaB-BCL2 axis represents a key pathway to cisplatin resistance in non-small cell lung cancer cells.
Rap1GAP functions as a novel suppressor of epithelial mesenchymal transformation and tumor metastasis in gastric cancer, and loss of Rap1GAP predicts poor prognosis.
The formation of the Rap1-TRF2 complex restored DNA unwinding.
Rap1 may induce hepatic ischemia reperfusion injury (IRI) through promoting neutrophils inflammatory response. Rap1 may be the potential therapeutic target of attenuating hepatic IRI.
The Rap1-RIAM-talin axis of integrin activation and blood cell function
Rap1 activation was dependent on PKA and required Src family kinases and the Rap1 exchanger C3G.
RAP1 promotes colorectal cell migration through the regulation of Vimentin and RAP1 may act as a potential target for the diagnosis and therapy of CRC.
Data show that isoform beta2 of the heregulin (HRGbeta2) localizes at telomeres with the telomere-associated proteins TRF2 and RAP1.
Data indicate telomere-binding protein RAP1 as an interacting partner of isoform beta2 of the heregulin (HRGbeta2).
In pro-inflammatory macrophages, Rap1 promotes cytokine production via NFkappaB activation favoring a pro-inflammatory environment which may contribute to the development and progression of atherosclerosis.
Through a combination of biochemical, biophysical and structural approaches, we unveiled a unique mode of assembly between RAP1 and TRF2
the conservation of Rap1 reflects its role in transcriptional regulation rather than a function at telomeres.
These findings reveal Pkp3 as a coordinator of desmosome and adherens junction assembly and maturation through its functional association with Rap1.
Data show that full-length repressor activator protein 1 (Rap1) binds to full-length telomeric repeat binding factor 2 (TRF2) with high affinity and equimolar ratio.
C3G/RAP1 activity is involved in the metastatic spread of epithelial ovarian cancer.
a detailed analysis of individual focal adhesion parameters identified focal adhesion size, sliding and intensity as primary targets of Rap1.
TBC1D21 may interact with and potentially regulate Rap1 during murine spermatogenesis.
HS1 as an important regulator of proper Rac1 and Rap1 activation and neutrophil extravasation.
Collectively the observations uncover a requirement for Rap1 in maintenance of lens epithelial phenotype and morphogenesis.
our results indicate that Rasa3 catalytic activity controls Rap1 activation and integrin signaling during megakaryocyte differentiation in mouse.
RASA3, inhibits platelet activation and provides a link between P2Y12 and activation of the RAP1 signaling pathway.
we summarize recent developments in understanding the small G protein RAP1 and its effector RASIP1 as critical mediators of endothelial junction stabilization.
Molecular investigation revealed that deletion of RAP1 reduced upregulation of inflammatory cytokine (IL1A), finely regulated the expression of angiogenic factor (VEGF), and antiangiogenic factor (PEDF), following injury for better corneal recovery.
Cdk5-mediated serine-phosphorylation of C3G may control Rap1 stability and activity
Mesenchymal high-grade glioma is maintained by the ID-RAP1 axis.
Rap1-Rac1 circuits potentiate platelet activation.
Mouse gene deletion experiments revealed DNA-damage-response pathways that threaten chromosome ends and how the components of the telomeric shelterin complex prevent activation of these pathways.[Shelterin]
Rap1-deficient meiotic telomeres assemble the SUN1 nuclear membrane protein, attach to the nuclear envelope, and undergo bouquet formation.
HPK1 competes with ADAP for SLP-76 binding and via Rap1 negatively affects T-cell adhesion.
Mice with Rap1 deletion in stratified epithelia were viable but had shorter telomeres and developed skin hyperpigmentation in adulthood.
Rap1-mutant mice display defective NF-kappaB activation and are resistant to endotoxic shock.
study found Rap1 dispensable for essential functions of TRF2--repression of ATM kinase signaling & NHEJ--& mice lacking telomeric Rap1 were viable & fertile; Rap1 was critical for the repression of homology-directed repair which can alter telomere length
The gene encodes a protein that is part of a complex involved in telomere length regulation. Pseudogenes are present on chromosomes 5 and 22.
, TERF2-interacting telomeric protein 1
, TRF2-interacting telomeric RAP1 protein
, TRF2-interacting telomeric protein 1
, dopamine receptor interacting protein 5
, dopamine receptor-interacting protein 5
, repressor/activator protein 1 homolog
, telomeric repeat-binding factor 2-interacting protein 1
, TRF2-interacting telomeric protein Rap1