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Validated All-in-One™ qPCR Primer for FGFR2(NM_000141.4) Search again
Product ID:
HQP096070
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BBDS, BEK, BFR-1, CD332, CEK3, CFD1, ECT1, JWS, K-SAM, KGFR, TK14, TK25
Gene Description:
fibroblast growth factor receptor 2
Target Gene Accession:
NM_000141.4(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 protein encoded by this gene is a member of the fibroblast growth factor receptor family, where amino acid sequence is highly conserved between members and throughout evolution. FGFR family members differ from one another in their ligand affinities and tissue distribution. A full-length representative protein consists of an extracellular region, composed of three immunoglobulin-like domains, a single hydrophobic membrane-spanning segment and a cytoplasmic tyrosine kinase domain. The extracellular portion of the protein interacts with fibroblast growth factors, setting in motion a cascade of downstream signals, ultimately influencing mitogenesis and differentiation. This particular family member is a high-affinity receptor for acidic, basic and/or keratinocyte growth factor, depending on the isoform. Mutations in this gene are associated with Crouzon syndrome, Pfeiffer syndrome, Craniosynostosis, Apert syndrome, Jackson-Weiss syndrome, Beare-Stevenson cutis gyrata syndrome, Saethre-Chotzen syndrome, and syndromic craniosynostosis. Multiple alternatively spliced transcript variants encoding different isoforms have been noted for this gene. [provided by RefSeq].
Gene References into function
- Associated with Pfeiffer syndrome
- vitronectin increased the presence of all four growth factor receptors and most notably, VEGFR-1; in contrast, fibrin decreased all four receptors, especially FGFR-1 and FGFR-2
- distribution in normal endocrine cells and related tumors of the gastroenteropancreatic system; immunoreactive in gastric and duodenal G cells, pancreatic B cells, and rectal EC cells
- genomic screening reveals a wide spectrum of mutations in patients with syndromic craniosynostosis
- genomic sequence and variations (SNPs)
- KGF induced proliferation but did not cause significant differentiation of 3 hematopoietic cell lines and bone marrow cells transduced with human K-sam.
- role of Ser351Cys mutation in causing craniosynostosis and sacral appendage
- details of the endocytic pathway followed by the keratinocyte growth factor receptor following activation by KGF binding
- Craniofacial dysostosis is associated with mutations of FGFR2 and is characterized by premature fusion of cranial sutures.
- FGFR2 has a role in controlling normal and premature cranial ossification in humans [review]
- Differences in spatial patterns of FGFR expression in normal skin may generate functional diversity in response to FGFs, and in wounded skin FGFs may function in wound healing via induced FGFRs.
- a nonsequence-specific double stranded RNA stem constitutes a functional element required for FGFR2 splicing
- A novel splice variant of FGFR2 (FGFR2AT-I) arising from skipping exons 7-10 was able to bind FGF1, FGF2, and FGF7, leading to loss of ligand binding specificity and increased AKT and MAPK activation, conferring a survival advantage.
- PAK4 interacts with KGF receptor and mediate anti-apoptosis effects of KGF on epithelial cells.
- FGFR2b is alternatively spliced and is activated by FGF7 and FGF10
- KGFR was localized in the vascular smoooth muscle cells in normal human coronary arteries and in the thickened intima of atherosclerotic arteries.
- mRNA splicing of fibroblast growth factor receptor 2 is associated with Chondrosarcoma
- This gene is expressed on chromosome 10p26.
- Data show that the HTPAPL-WDR11-FGFR2 locus was more susceptible to recombination than to nucleotide substitution.
- physical association of p63alpha and ABBP1 led to a specific shift of FGFR-2 alternative splicing toward the K-SAM isoform essential for epithelial differentiation
- proposed that the FGFR2 mutations, although harmful to embryonic development, are paradoxically enriched because they confer a selective advantage to the spermatogonial cells in which they arise
- Activation of iFGFR1, but not iFGFR2, led to strong up-regulation of osteopontin in prostate adenocarcinoma.
- regulated splicing of fibroblast growth factor receptor-2 transcripts leads to tissue-specific expression of distinct receptor isoforms
- KGFR was prominently localized in proliferating reserve cells and squamous metaplastic reserve cells adjacent to cancer cells. In contrast, KGFR was not detected in cervical ductal cells in cancer or non-cancer cervical tissues.
- FGFR2 activation induces osteoblast differentiation by Cbl-mediated degradation of Lyn and Fyn
- A point mutation in fibroblast growth factor receptor 2 (FGFR2) was identified that had previously been seen only in sporadic cases of Crouzon syndrome.
- Elevated Apert syndrome mutant FGFR2b signaling may account for the dermatological manifestations of Apert syndrome
- Osteocalcin mRNA was down-regulated in Apert osteoblasts carrying the FGFR2 P253R mutation, Runt-related transcription factor-2 (RUNX2) mRNA was differentially spliced, and FGF2 secretion was greater.
- inhibits the growth of bladder carcinoma cells by reducing IGF-II levels via its carboxy-terminal domain, independent of its tyrosine kinase activity
- Missense substitution in FGFR2 is associated with Crouzon syndrome
- FGFR2 is a transforming oncogene in human mammary epithelial cells when expressed to levels similar to that found in breast cancer cells with FGFR2 gene amplification.
- in-frame insertion in exon 8 reported in a child with Crouzon's syndrome, tracheal anomalies, and a tail
- In 'undifferentiated' neurospheres of embryonic brain and spinal cord, transcripts from FGFR1 and FGFR2 were consistently detected.
- Review. Advances in understanding the molecular basis for Apert syndrome through clinical genetic, biochemical, & structural approaches of FGFR2 are reviewed.
- Data validate the symmetric two-end model of fibroblast growth factor (FGF) receptor (FGFR) dimerization and FGF binding and argue against the asymmetric model of FGFR dimerization.
- These findings indicate that KGFR may play important roles in the differentiation of normal colorectal epithelial cells and establishment of the well-differentiated histological type of colorectal cancer cells.
- the alpha5 integrin subunit has a role in the induction of apoptosis triggered by FGFR2 activation in osteoblasts, and a Cbl-dependent mechanism is involved in the coordinated regulation of cell apoptosis induced by alpha5 integrin degradation
- Alleleic loss at 10q26 in osteosarcoma is reported in the region of FGFR2.
- provides genetic and biochemical evidence for a role of Fgfr2 in the altered osteoblast phenotype induced by Twist haploinsufficiency in Saethre-Chotzen syndrome
- FGFR2 mutations attain high levels in sperm because they encode proteins with gain-of-function properties, favoring clonal expansion of mutant spermatogonial cells.
- Igfbp5-mediated fibroblast growth factor receptor 2-IIIb signals regulate the genetic program that controls the structure of the hair shaft medulla in transgenic mice.
- Altered expression is associated with therapy failure and death in patients with multiple types of cancer.
- FGFR2 mutations are responsible for causing a familial scaphocephaly syndrome with almost exclusive involvement of the sagittal suture.
- Data indicate that after endocytosis, fibroblast growth factor receptor (FGFR)4 and its bound ligand, FGF1, are sorted mainly to the recycling compartment, whereas FGFR1-3 with ligand are sorted mainly to degradation in the lysosomes.
- KGFR expression was upregulated in ADPKD kidney tissues.
- Stimulation of FGFR-2 results in a Ca2+ channel-dependent stimulation of VEGF secretion in retinal pigment epithelial cells.
- For the first time in humans, the expression of basic fibroblast growth factor (bFGF) and its receptors FGFR-2, FGFR-3, and FGFR-4 has been documented in ovaries of second- and third-trimester fetuses.
- expression of hepatocyte and keratinocyte growth factors and their receptors is preserved in patients with lung emphysema as compared to patients without emphysema
- studied the capacities of a variety of heparin oligosaccharides to bind FGF1 and FGFR2c both separately and together in ternary complexes. In the absence of heparin, FGF1 had no detectable affinity for FGFR2c
- specific glycosaminoglycans inhibit or activate Apert syndrome FGFR2 (S252W) signaling
- a limited number of recurrent FGFR2 mutations accounts for severe forms of Pfeiffer syndrome
- FGFR2 gene mutation is involved in Apert syndrome with preaxial polydactyly.
- analysis of heparan sulfate-related oligosaccharide binding to fibroblast growth factors 1 and 2 and their receptors
- FGFR2-IIIb expression in HaCaT keratinocytes corresponds with the proliferative activation of the cells and is not related to the differentiation programme
- autoactive FGFR2 can signal from intracellular compartments
- Evaluation by immunohistochemistry of KGF receptor distribution, showed a down-modulation of this receptor, as previously reported in the presence of increased levels of KGF clear cell acanthoma (CCA).
- We therefore conclude that aberrant expression of alternatively spliced isoforms of FGFR2 with the C3 carboxyl terminus in the SUM-52 breast cancer cells results in sustained activation of signal transduction leading to transformation.
- Apert syndrome, a disorder of craniosynostosis, syndactyly, and other craniofacial malformations, is caused by point mutations (Ser252Trp or Pro253Arg) in the fibroblast growth factor receptor 2 gene.
- FGFR2 mutations may play a role in tumorigenesis.
- there was a differential effect of FGFR2 mutations in ophthalmic findings in patients with Apert syndrome, with significantly greater prevalence of visual impairment in the Ser252Trp mutation compared with the Pro253Arg mutation
- These results indicate that mutations are rare in FGF8 and FGFR2 in hypospadias, but gene variants may influence the risk.
- no evidence that mosaicism for mutations, normally associated with syndromal forms of craniosynostosis, occur in single suture craniosynostosis
- This is the 8th report of Beare-Stevenson syndrome in the literature, which was confirmed by the detection of a Tyr375Cys mutation in the fibroblast growth factor receptor 2 (FGFR2) gene.
- KGF triggers negative feedback between ERK1/2 and AKT pathways to regulate cell proliferation/differention.
- Thus, our results suggest that the epigenetic silencing of FGFR2 through DNA methylation in gastric cancer may contribute to tumor progression.
- Aberrant expression of keratinocyte growth factor receptor in ovarian surface epithelial cells of endometrioma.
- Our in vivo data, taken together with previous in vitro results, show that K-SAM splicing activation involves cooperative binding of TIA-1 and U1 snRNP to the exon's 5' splice site region.
- Data show that enhanced expression of keratinocyte growth factor and its receptor correlates with venous invasion in pancreatic cancer.
- identification of a total of 11 different FGFR2 mutations in 3/10 (30%) of endometrial cell lines and 19/187 (10%) of primary uterine tumors
- Four single nucleotide polymorphisms in intron 2 of FGFR2 are highly associated with sporadic postmenopausal breast cancer.
- study of cellular mechanisms underlying Apert phenotype, by analyzing effects of FGF2 in cultures of Apert periosteal fibroblasts carrying the FGFR2 Pro253Arg mutation
- FGF receptor 1 (FGFR1), which is expressed mainly in neoplastic thyroid cells, propagates MAPK activation and promotes tumor progression. In contrast, FGFR2 is down-regulated in neoplastic thyroid cells through DNA promoter methylation.
- Osteogenic potential of Apert syndrome periosteal cells with FGFR2 p.Ser252Trp mutation was tested;these cells are more committed toward the osteoblast lineage.
- Results suggest that Lacrimo-auriculo-dento-digital syndrome is caused by reduced activity of the fibroblast growth factor 10 (FGF10)-FGF receptor 2 signaling pathway.
- expression of the keratinocyte growth factor receptor was up-regulated in early stages of liver fibrosis and down-regulated in cirrhotic organs
- Gene expression profiling identified the cancer/testis antigen MAGE-A3/6 as a novel target of FGFR2-IIIb signaling.
- rejection of the hot spot model and lack of rejection of a selection model for the C755G mutation supports the view that positive selection in the testis can act to increase the frequency of premeiotic germ cells carrying a mutation harmful to offspring
- Comparison of the crystal structures of unphosphorylated and phosphorylated wild-type FGFR2 kinase domains with those of pathogenic mutants reveals an autoinhibitory "molecular brake" mediated by a triad of residues in the kinase hinge region.
- a mutation in the fibroblast growth factor receptor (FGFR)-2 gene may have a role in endocardial cushion defect in a patient with Crouzon syndrome [case report]
- KGFR internalization triggered by either KGF or FGF10 occurs through clathrin-coated pits
- Correlation between the number of minor alleles of rs2981582 in FGFR2 and the average number of first-degree and second-degree relatives with breast cancer and/or ovarian cancer (P = 0.05).
- findings support the hypothesis that the W290C mutation in FGFR2 is associated with a severe phenotype in Pfeiffer syndrome
- FGFR2 uses a less stringent mode of autoinhibition than FGFR1
- No sequence variation was found, indicating that mutations in the "hot spot" exons are not associated with nonsynostotic plagiocephaly.
- case of Beare-Stevenson syndrome with an FGFR2 Ser372Cys mutation.
- Common variation in the breast-cancer implicated intron 2 and other highly plausible causative candidate regions of FGFR2 do not appear to be a major contributor to endometriosis susceptibility in our large Australian sample.
- An FGFR2 splice variant is expressed in breast carcinoma cell lines, with a specific splice variant expressesed in invasive breast carcinomas.
- The differences in the effects of the FGFR2 and MAP3K1 SNPs between BRCA1 and BRCA2 carriers point to differences in the biology of BRCA1 and BRCA2 breast cancer tumors and confirm the distinct nature of breast cancer in BRCA1 mutation carriers.
- These observations suggest that the altered FRS2 recruitment by the mutant receptors results in an abnormal cellular signalling mechanism.
- Results identify a molecular mechanism by which activated FGFR2 recruits Cbl in raft micro-domains to trigger PI3K ubiquitination and proteasome degradation, and reveal a role for PI3K/Akt in the control of osteoblast survival by FGFR2 signaling.
- Results reveal that both the FGFR2 and EGFR family signaling pathways are activated in FGFR2-amplified gastric cancer cell lines to drive cell proliferation and survival.
- Results demonstrate altered expression of two isoforms, FGFR2-IIIb and FGFR2-IIIc in dermatofibroma lesions.
- summary of the effects of FGFR2 and Twist genetic mutations resulting in altered osteoblast phenotype and premature cranial fusion based on analysis in human syndromic craniosynostosis [review]
- FGFR2 gene mutation is responsible for the pathogenesis of Crouzon syndrome in these patients.
- two cis-regulatory SNPs alter binding affinity for transcription factors Oct-1/Runx2 and C/EBPbeta, and synergize to give rise to increased FGFR2 expression, thereby possibly increasing the propensity for tumour formation
- FGFR2 is a breast cancer susceptibility gene in Jewish and Arab Israeli populations.
- These results establish hnRNP H and hnRNP F as being repressors of exon inclusion and suggest that Fox proteins enhance their ability to antagonize ASF/SF2.
- An FGFR2 mutation was found in a patient with Crouzon syndrome and a sacral appendage.
- FGFR2ome analyses in patients with several tumor types among various populations should be carried out to establish integrative database of FGFR2 for the rational clinical application of FGFR2-targeted cancer therapy.
- A lethal point mutation was found in FGFR2 in a fetus with Pfeiffer syndrome and multiple pterygia.
- data suggest that inhibition of FGFR2 may be a viable therapeutic option in endometrial tumors possessing activating mutations in FGFR2, despite the frequent abrogation of PTEN in this cancer type
- blockage of FGF-2 in the co-cultures or the genetic or pharmacological inhibition of FGFR-2 inhibited progesterone receptors activation and tumor cell proliferation
- There is an overexpression of the fibroblast growth factor receptor 2-IIIc in Kaposi's sarcoma.
- bFGF, FGFR1, and FGFR2 are frequently overexpressed in squamous cell carcinoma and adenocarcinoma of the lung and may have a role in neoplasm pathogenesis
- MAGE A3 is a functional integrator of diverse signals, including FGFR2 and FN, to modulate cancer progression.
- The recruitment of Shc protein to FGFR2 via an indirect mechanism provides new insight into the regulation of protein assembly and activation of various signalling pathways.
- genetic variants in FGFR2 may contribute to breast cancer occurrence in Chinese women
- FGFR2 and MAP3K1 are involved in breast cancer susceptibility and confer their effects primarily in ER+ and PR+ tumors.
- The crystal structure of the FGF receptor 2 kinases caught in the act of trans-phosphorylation of Y769, the major C-terminal phosphorylation sitem, is presented.
- 10% of melanoma tumors and cell lines harbor mutations in the fibroblast growth factor receptor 2 (FGFR2) gene.
- Signaling of transgenic Fgfr1 and Fgfr2 is important for their potential ability to mediate axon-glial interaction in the peripheral sensory pain pathway, via influencing myelinating and nonmyelinating Schwann cell function.
- ESRP1 and ESRP2 are epithelial cell-type-specific regulators of FGFR2 splicing.