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Validated All-in-One™ qPCR Primer for RAP1A(NM_001010935.2) Search again
Product ID:
HQP016103
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
C21KG, G-22K, KREV-1, KREV1, RAP1, SMGP21
Gene Description:
RAP1A, member of RAS oncogene family
Target Gene Accession:
NM_001010935.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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. [provided by RefSeq].
Gene References into function
- Consequences of mevalonate depletion. Differential transcriptional, translational, and post-translational up-regulation
- ERK activation by cAMP does not require RAP1
- role in regulating phorbol 12-myristate 13-acetate-stimulated but not ligand-induced beta 1 integrin-dependent leukocyte adhesion
- Galpha and Gbeta gamma require distinct Src-dependent pathways for its activation
- Rap1 may represent a critical control point in the stromal inhibition of megakaryoytic differentiation.
- cAMP inhibits both Ras and Rap1 activation in primary human T lymphocytes, but only Ras inhibition correlates with blockade of cell cycle progression.
- rap1 inhibits proliferation in keratinocytes
- RAP1A is prominently expressed in the nucleus of squamous carcinomas.
- inherited Rap1 activation defect associated with a pathologic disorder in leukocyte integrin function; we herein term it LAD-III, leukocyte adhesion deficiency syndrome
- Eph/ephrin signaling enhances the ability of platelet agonists to cause aggregation provided that those agonists can increase cytosolic Ca(++) and this is accomplished in part by activating Rap1
- Rap1 GTPase has functions in malignancy (review)
- Results suggest that membrane localizations of Rap1 are dynamically regulated, and the cell membrane is the principle platform from which Rap1 signaling emanates.
- a previously uncharacterized domain spanning amino acids 85-89 of Rap1A plays a pivotal role in its perinuclear localization and acts dominantly over COOH-terminal lipid modification of Ha-Ras
- mRNA expression of Rap1A protein in the spermatogenic cells of azoospermic was stronger than that in those of the fertile testes
- Rap1 plays a vital role in the establishment of E-cadherin-based cell-cell adhesion
- cAMP-Epac-Rap1 pathway regulates cell spreading and cell adhesion to laminin-5 through the alpha3beta1 integrin but not the alpha6beta4 integrin
- Activation of Epac results in markedly enhanced basal endothelial barrier function by increasing cortical actin and subsequent redistribution of adherens and tight junctional molecules to cell-cell contacts
- Rap1 promotes cell spreading by localizing a subset of Rac GEFs to sites of active lamellipodia extension
- Rap1 activation contributes to directional vascular endothelial cell migration accompanied by extension of microtubules on which RAPL localizes
- MAP1A LC2 is a biological enhancer of EPAC1 activity toward Rap1 and associated downstream signaling mechanisms
- cAMP-Epac-Rap1 signaling promotes decreased cell permeability by enhancing VE-cadherin-mediated adhesion lined by the rearranged cortical actin
- Epac-mediated Rap1 activation may represent an important signaling pathway for promoting sickle cell adhesion.
- the G(alpha)o/i-coupled cannabinoid receptor, by regulating the proteasomal degradation of Rap1GAPII, activates Rap1 to induce neurite outgrowth.
- Rap1 GTPase inhibits leukocyte transmigration by promoting endothelial barrier function.
- JAM1 regulates epithelial cell morphology and beta1 integrin expression by modulating activity of the small GTPase Rap1.
- cGKI inhibited ADP-induced Rap 1 activation induced by the Galpha(i)-coupled P2Y12 receptor alone, i.e. independently of effects on Ca2+-signalling
- On ephrinB1 stimulation, the small GTPases Rho and Ras are activated and Rap1 is inactivated.
- The RAP1A gene mutation is a rare event in myelodysplastic syndromes(MDS) bone marrow cells.
- first evidence of an E-cadherin-modulated endosomal signaling pathway involving Rap1, and suggest that cadherins may have a novel modulatory role in integrin adhesive functions by fine-tuning Rap1 activation
- RT-PCR analysis of mRNA extracted from highly purified reticulocytes confirmed the expression of Rap2b, but not Rap2a, Rap2c, Rap1a or Rap1b.
- TIMP-2 mediated alteration in cell morphology requires Rap1, TIMP-2 may recruit Rap1 to sites of actin cytoskeleton remodeling necessary for cell spreading, and enhanced cell adhesion by TIMP-2 expression may hinder cell migration
- The Epac1-Rap1 pathway is present in both monocytes and macrophages, but only regulates specific immune effector functions
- Results suggest that Dok-4, through activation of the Rap1-ERK1/2 pathway, regulates GDNF-mediated neurite outgrowth during neuronal development.
- The patients with emphysema had significantly higher percentages of type II cells positive for p16INK4a and p21CIP1/WAF1/Sdi1 than the asymptomatic smokers and nonsmokers.
- A study that demonstrated the engagement of beta2 integrins on human neutrophils increased the levels of GTP-bound Rap1 and Rap2 is presented.
- Rap1 mediates cyclic AMP-stimulated neurotensin secretion downstream of both Epac and protein kinase A signaling pathways
- While Rap1GAP(N290A) is completely inactive on wild-type Rap1, it can act on Rap1(T61Q), arguing that Asn290 in trans has a role in catalysis similar to that of the intrinsic Gln in Ras and Rho.
- These findings raise the possibility that Rgl3 mediates interaction between Ras/Rap-family proteins and profilin II, an important activator of actin polymerization.
- Rap1 regulates malignant transformation mechanisms of hematopoietic progenitors
- IQGAP1 may link the calmodulin and Rap1 signaling pathways
- Essential role for Rap1 GTPase and its guanine exchange factor CalDAG-GEFI in LFA-1 mediated human T-cell adhesion.
- interaction surfaces in RAPL-Rap1 and RAPL-Rap2 complexes are different and that a single residue in the switch I region of Rap proteins (residue 39) contributes considerably to the different kinetics of these protein-protein interactions.
- Epac1 was shown to be responsible for these actin changes and to colocalize with microtubules in human umbilical vein endothelial cells.
- activation of functional alpha(4) integrin activity in resting eosinophils is mediated by Rap1 provided that the intracellular-free Ca(2+) is at a normal homeostatic concentration
- Cyclic AMP acts through Rap1 and JNK signaling to increase expression of cutaneous smooth muscle alpha2C-adrenoceptors.
- Results suggest that Rap1a is a key regulator of fibroblast growth factor 2-induced angiogenesis and together with Rap1b controls endothelial cell functions.
- The beta2 integrin-dependent exocytosis of specific and gelatinase B-containing granules is responsible for the translocation of Rap1 and Rap2 to the plasma membrane in human neutrophils.
- Rap1a and Rap1b are essential for the conformational activation of beta1-integrins in endothelial cells
- Results identify a mechanism by which the WAVE2 complex regulates T cell receptor signaling to Rap1 and integrin activation via Abl- and CrkL-C3G.
- Rap1 and its exchange factor C3G in mediating Fc gammaR-dependent phagocytosis.
- Rap1 as another downstream target of the Abl-CrkII signaling module and show that Abl-CrkII collaborates with Rho-ROCK1 to stimulate cell retraction.