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Validated All-in-One™ qPCR Primer for AXIN1(NM_003502.3) Search again
Product ID:
HQP020114
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AXIN, PPP1R49
Gene Description:
axin 1
Target Gene Accession:
NM_003502.3(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
This gene encodes a cytoplasmic protein which contains a regulation of G-protein signaling (RGS) domain and a dishevelled and axin (DIX) domain. The encoded protein interacts with adenomatosis polyposis coli, catenin (cadherin-associated protein), beta 1, 88kDa, glycogen synthase kinase 3 beta, protein phosphate 2, and itself. This protein functions as a negative regulator of the wingless-type MMTV integration site family, member 1 (WNT) signaling pathway and can induce apoptosis. The crystal structure of a portion of this protein, alone and in a complex with other proteins, has been resolved. Mutations in this gene have been associated with hepatocellular carcinoma, hepatoblastomas, ovarian endometriod adenocarcinomas, and medullablastomas. Two transcript variants encoding distinct isoforms have been identified for this gene. [provided by RefSeq].
Gene References into function
- Axin-mediated CKI phosphorylation of beta-catenin at Ser 45: a molecular switch for the Wnt pathway.
- Overexpression of Icat induces G(2) arrest and cell death in tumor cell mutants for adenomatous polyposis coli, beta-catenin, or Axin.
- Role of Wnt pathway in medulloblastoma oncogenesis: accumulation of beta-catenin in tumor cells was immunohistochemically proven in 5 cases; 2 cases showed positive immunoreactivity for Wnt-1 and another 2 showed mutation of either CTNNB1 or AXIN1
- Data report the crystal structure of glycogen synthase kinase 3beta (GSK3beta) in complex with a minimal GSK3beta-binding segment of axin, at 2.4 A resolution.
- identification of mutations but not deletions in cerebellar medulloblastomas
- In mice, ectopic expression of Axin1, an inhibitor of the Wnt signalling pathway, restricts haematopoietic stem cell (HSC) growth in vitro and reduces reconstitution in vivo.
- Reduced expression of Axin correlates with tumour progression of esophageal squamous cell carcinoma
- mutations of AXIN1 may play a limited role in tumorigenesis of cervical cancer
- a tumor-associated mutation of the Axin gene is generally a rare event in pediatric neoplasms
- The missense mutation rate is 11%, suggesting that Axin deficiency may contribute to the onset of colorectal tumorigenesis.
- Axin binds directly to the export factor CRM1 in the presence of RanGTP
- neither AXIN1 gene mutations nor AXIN1 locus LOH are involved in Wnt pathway activation in gastroesophageal junction adenocarcinomas
- We also found that cyclin A/CDK2 phosphorylates Axin, thereby enhancing its association with beta-catenin.
- In the presence of p53, the movement of Axin into & out of the Triton X-100-insoluble fraction is accelerated. p53 induces a faster mobilization of Axin into the degradation complex
- Ccd1 drastically inhibited JNK activation both by Axin and by Dvl.
- APC is down-regulated by the ubiquitin-proteasome pathway in a process facilitated by Axin
- Axin acts as a tumor suppressor by facilitating p53 function
- Axin forms homodimeric interactions through three domains, D, I, and DIX
- Beta-catenin stabilization because of either beta-catenin or AXIN I mutation might be a late event for malignant progression rather than an early genetic event involving the initiation of HCC development.
- No significant genetic alterations were found.
- Axin1 gene may be one of the mutational target in oral SCC.
- Axin and Arkadia cooperate with each other in promoting Smad7 ubiquitination.
- Splice forms of crucial genes of the Wnt-pathway, beta-Catenin, LRP5, GSK3beta, Axin-1 and CtBP1 are expressed in human colorectal tissue.
- findings raise the possibility that hypermethylation of the AXIN1 promoter, by mechanisms as yet undetermined, is associated with caudal duplication
- These findings establish that the RGS domain of axin is able to directly interact with the alpha subunit of heterotrimeric G protein G12 and provide a unique tool to interdict Galpha12-mediated signaling processes.
- Data show that P68 RNA helicase mediates platelet-derived growth factor-induced epithelial mesenchymal transition by displacing Axin from beta-catenin.
- AXIN1, AXIN2 and TCF7L2 may have roles in development of colorectal carcinomas [review]
- The retained beta-catenin in cytoplasm by APC may be down-regulated by Axin 2, which is induced by beta-catenin/Tcf signaling.
- The activation of p38 was dependent on Axin and was required for the enhancement of mesenchymal stem cells differentiation by Wnt-4.
- Reduced expression of axin is associated with the development of lung cancer
- activation of Wnt signaling through AXIN1 rather than beta-catenin mutation might play an important role in liver carcinogenesis.
- Mutations in AXIN1 and AXIN2 may contribute to gastric carcinogenesis.
- the C6 motif seems to reduce the interaction of Axin with Dvl-1.
- A novel role for the tumour suppressor scaffold protein Axin1 in facilitating the formation of a degradation complex for c-Myc containing GSK3beta, Pin1, and PP2A-B56alpha is reported.