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Validated All-in-One™ qPCR Primer for RET(NM_020975.6) Search again
Product ID:
HQP160111
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CDHF12, CDHR16, HSCR1, MEN2A, MEN2B, MTC1, PTC, RET-ELE1
Gene Description:
ret proto-oncogene
Target Gene Accession:
NM_020975.6(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, a member of the cadherin superfamily, encodes one of the receptor tyrosine kinases, which are cell-surface molecules that transduce signals for cell growth and differentiation. This gene plays a crucial role in neural crest development, and it can undergo oncogenic activation in vivo and in vitro by cytogenetic rearrangement. Mutations in this gene are associated with the disorders multiple endocrine neoplasia, type IIA, multiple endocrine neoplasia, type IIB, Hirschsprung disease, and medullary thyroid carcinoma. Two transcript variants encoding different isoforms have been found for this gene. Additional transcript variants have been described but their biological validity has not been confirmed. [provided by RefSeq].
Gene References into function
- The presence of coiled-coil domains in the ktn1/ret fusion protein (PTC8) suggests ligand-independent dimerization and thus constitutive activation of the ret tyrosine kinase domain.
- Three new somatic cell missense mutations of the RET proto-oncogene associated with sporadic medullary thyroid carcinoma (MTC).
- A germline RET mutation at codon 603 in exon 10 is associated with both medullary and nonmedullary thyroid cancer in a kindred.
- Differentiation of cardiac ganglionic cells is affected, after RETINOIC ACID treatment, by the down-regulation of c-Ret.
- RET oligonucleotide microarray for the detection of RET mutations in multiple endocrine neoplasia type 2 syndromes
- The finding of a somatic deletion in RET exon 15 clarified the sporadic nature of a medullary thyroid carcinoma suspected to be familial. A 12 bp deletion within the catalytic domain of the protooncogene RET.
- role in regulating rac activity and lamellipodia formation
- early detection of RET proto-oncogene mutation is crucial for prevention of thyroidectomy in multiple endocrine neoplasia type 2 children
- if the association between Hashimoto's thyroiditis and thyroid cancer exists, its molecular basis is different from RET/PTC rearrangement
- Familial medullary thyroid carcinoma: clinical variability and low aggressiveness associated with RET mutation at codon 804.
- family in which the MEN 2A and the HSCR phenotypes are associated with a single point mutation in exon 10 of the RET proto-oncogene. polymorphic sequence variants of the RET proto-oncogene.
- germline mutation of the RET proto-oncogene in members of Slovak families with multiple endocrine neoplasia 2
- Segregation at three loci explains familial and population risk in Hirschsprung disease. We show oligogenic inheritance of S-HSCR, the 3p21 and 19q12 loci as RET-dependent modifiers, and a parent-of-origin effect at RET.
- Dissecting Hirschsprung disease. RET is the main gene conferring susceptibility.
- These observations lend support to the idea that both RET alleles have a role in pathogenesis of Hirschsprung's disease, in a dose-dependent fashion. We also showed that the c135G/A polymorphism modifies the phenotype.
- Hirschsprung associated GDNF mutations do not prevent RET activation
- the G691S and S904S variants of RET may somehow play a role on the age of onset of MEN 2A
- Activation of RET tyrosine kinase regulates interleukin-8 production by multiple signaling pathways
- RET activation closely parallels the morphological changes, that it is restricted to those areas of the tumor with the cytological alterations and that it is detectable in both mono- and polyclonal tumors
- RET codon 691 polymorphism is associated with radiation induced tumors with a C-cell hyperplasia of thyroid tumors
- RET/PTC rearrangement in thyroid tumors. Review
- RET expression in papillary thyroid cancer from patients irradiated in childhood for benign conditions.
- Analysis of mutation of protooncogene RET are presented in patients with thyroid medullary carcinoma
- analysis of RET somatic mutations supports the differentiation between sporadic and inherited medullary thyroid carcinoma
- 5'-End RET splicing: absence of variants in normal tissues and intron retention in pheochromocytomas.
- Possible pathogenesis of papillary thyroid carcinoma caused by exon 13 and 14 RET mutations that affect the intracellular domain of ret proto-oncogene protein.
- a protective role of this low-penetrant haplotype in the pathogenesis of HSCR and demonstrate a possible functional effect linked to RET messenger RNA expression.
- genetic interaction between mutations in RET and EDNRB is an underlying mechanism for Hirschsprung disease
- relationship between RET oncogene and Chinese patients with Hirschsprung's disease
- A novel Val648Ile substitution in RET protooncogene observed in a Cys634Arg multiple endocrine neoplasia type 2A kindred presenting with an adrenocorticotropin-producing pheochromocytoma.
- A founding locus within the RET proto-oncogene may account for a large proportion of apparently sporadic Hirschsprung disease and a subset of cases of sporadic medullary thyroid carcinoma
- Patients with RET codon 790/791 mutations seemed to have a less aggressive clinical course compared with patients with classic multiple endocrine neoplasia type 2A syndrome.
- Amplification and overexpression of mutant RET in multiple endocrine neoplasia type 2-associated medullary thyroid carcinoma. RET germline mutation in codon 634. Tandem duplication.Genomic chromosome 10 abnormalities increase mutant RET mRNA.
- RET proto-oncogene is often stimulated in follicular cell-derived thyroid tumors, not only in papillary carcinoma but also in follicular tumors (follicular adenomas and follicular carcinoma), and may contribute to tumorigenesis of these tumors.
- Not only RET mutations but also RET polymorphic variants may contribute to the occurrence of total intestinal aganglionosis.
- RET/PTC associates with STAT3 and activates it by the specific phosphorylation of the tyrosine 705 residue. STAT3 activation by the RET/PTC tyrosine kinase is one of the critical signaling pathways for the regulation of specific genes.
- High prevalence of BRAF mutations in thyroid cancer is genetic evidence for constitutive activation of the RET/PTC-RAS-BRAF signaling pathway in papillary thyroid carcinoma.
- in RET mutation carriers in Hirschsprung's disease, the gut caliber change was almost identical to the histologic transition in cases of short segment aganglionosis, whereas these were markedly dissociated in cases exhibiting extensive aganglionosis
- RET rearrangements may not play any distinctive role in driving histotype development and cancer progression in papillary thyroid carcinomas.
- A deletion of the chromosomal region including the RET proto-oncogene is involved in the pathogenesis of SCLC
- Specific nucleotide and amino acid exchanges at codon 634 might have a direct impact on tumor aggressiveness in MEN 2A.
- Letter discussing RET mutations in distinguishing between sporadic and familial medullary thyroid carcinoma.
- Four novel intronic mutations that have a strong association with the HSCR phenotype were identified in Hirschsprung disease patients
- The BRAF(V599E) mutation appears to be an alternative event to RET/PTC rearrangement rather than to RAS mutations, which are rare in PTC. BRAF(V599E) may represent an alternative pathway to oncogenic MAPK activation in PTCs without RET/PTC activation.
- mutations of the RET protooncogene were analyzed in Russian patients with inherited or sporadic medullary thyroid carcinoma.The most common mutation affected codon 918 to cause substitution of methionine with threonine and accounted for 31.6% alleles.
- findings support the notion that both RET alleles are involved in the pathogenesis of a subgroup of Hirschsprung disease patients in a dose-dependent fashion
- Shp2 activity required for RetM918T-induced Akt activation. Shp2 downstream mediator of mutated receptors RetC634Y and RetM918T. Shp2 acts as limiting factor in Ret-associated endocrine tumors, in neoplastic syndromes multiple endocrine neoplasia.
- there is a low-penetrance pheochromocytoma susceptibility locus in a region upstream of the putative loci for Hirschprung disease and apparently sporadic thyroid carcinoma.
- Point mutation in exon 14 at codon 804 of the RET proto-oncogene locus in a case of lymph node metastases of medullary and papillary thyroid carcinoma.
- Loss-of-function germline mutations of the RET proto-oncogene are reported in familial and sporadic cases of Hirschsprung disease (HSCR) with a variable frequency
- new missense point mutation in exon 8 of the RET gene (1597G-->T) corresponding to a Gly(533)Cys substitution in the cysteine-rich domain of RET protein
- Mass spectrometric analysis revealed that RET Tyr(806), Tyr(809), Tyr(900), Tyr(905), Tyr(981), Tyr(1062), Tyr(1090), and Tyr(1096) were autophosphorylation sites.
- association of high-level Ret proto-oncogene protein expression with neuronal morphology suggests that the variable overexpression of Ret in pheochromocytomas might in part be an epiphenomenon, reflecting the known phenotypic plasticity of these tumors
- Ret expression is significantly higher in thyroid papillary carcinoma than benign thyroid tissue; and this characteristic can have important diagnostic value.
- Ret tyrosine 981 constitutes the major binding site of the Src homology 2 domain of Src and therefore the primary residue responsible for Src activation upon Ret engagement
- Expression of the mitogenic and invasive phenotype of RET/PTC-transformed thyroid cells is stimulated by osteopontin.
- Data report the crystal structure of GFRalpha1 domain 3, and the effects of specific mutations on GDNF binding and RET phosphorylation.
- association of RET IVS1-126G>T variant with sporadic medullary thyroid cancer in a cohort of 104 patients
- Persephin/GFRalpha4 is unable to recruit RET protein into lipid rafts.
- RET expression leads to increased HSF1 activation, which correlates with increased expression of stress response genes. RET may be directly responsible for expression of stress response proteins and the initiation of stress response.
- With this study we excluded influence of the G691S polymorphism on RET mRNA expression, development of somatic RET mutation, the linkage with germline RET mutation, younger onset of medullary thyroid carcinoma, and clinical outcome of the disease.
- mutated in papillary thyroid cancer.
- RET point mutants for follicular thyroid cells may account for the occurrence of papillary thyroid carcinoma in patients affected by familial medullary thyroid carcinoma
- Dok-6 binds to the phosphorylated Ret Tyr(1062) residue resulting in phosphorylation of tyrosine residue(s) located within the unique C terminus of Dok-6 predominantly through a Src-dependent mechanism
- RET/PTC expression phosphorylates the Y701 residue of STAT1, a type II interferon (IFN)-responsive protein.
- Selective disruption of oncogenic RET signaling in medullary thyroid carcinoma in vitro and in vivo is associated with loss of the neoplastic phenotype of medullary thyroid carcinoma.
- the RET proto-oncogene mutation Y791F, characterized by a low penetrance, occurs comparatively frequently among patients with normal serum calcitonin concentrations
- mechanisms leading to RET oncogenic conversion
- RET requires coupling of Gab1 to phosphatidylinositol 3-kinase for function in human tumor cells
- Germ-Line Mutation in RET proto-oncogene is associated with Multiple Endocrine Neoplasia
- All Ret dominant-negative/+ mice died by 1 month of age and had distal intestinal aganglionosis reminiscent of Hirschsprung disease (HSCR) in humans
- critical role of the immunoglobulin domain in regulation of the localization of human PTPmu in bovine cell lines
- Papillary carcinomas with high RET/PTC1 expression showed an association trend for large tumor size.
- The Cys630 RET genotype may have a more vigorous transforming activity than currently thought and can cause medullary thyroid carcinoma in RET gene carriers within the first year of life.
- RET has roles in neoplastic transformation [review]
- Expression of a human Ret proto-oncogene with the MEN 2B mutation does not cause any features of MEN 2B in mice.
- Mutations of RET proto-oncogene may play an important role in the pathogenesis of Chinese patients with Hirschsprung disease.
- A RET haplotype (A-C-A) composed of alleles at three SNPs is associated with reduced RET gene expression in Hirschsprung patients.
- RET signals through focal adhesion kinase in medullary thyroid cancer cells.
- These findings establish a mechanism for the differential down-regulation of RET9 and RET51 signaling that could explain the apparently paradoxical activities of these two RET isoforms.
- RET/PTC and CK19 have roles in progression of papillary thyroid carcinoma
- RET gene mutation may explain the wide clinical variability associated with germline mutations at codon 804 in medullary thyroid carcinoma/multiple endocrine neoplasia type 2A patients.
- Single nucleotide polymorphisms in the RET oncogene may play a role in sporadic papillary thyroid carcinoma.
- Of these 86 variations, 8 proved to be in regions highly conserved among different vertebrates and within putative transcription factor binding sites. We therefore considered these as candidate disease-associated variants.
- Data show that the the RET receptor (RET/PTC), Ras and BRAF function along a linear oncogenic signaling cascade in which RET/PTC induces RAS-dependent BRAF activation and RAS- and BRAF-dependent ERK activation.
- Nuclease-resistant aptamers that recognize the human receptor tyrosine kinase RET were obtained using RET-expressing cells as targets in a modified random pool of sequences.
- Koreans showed increased RET gene expression in papillary thyroid carcinoma.
- a common non-coding RET variant within a conserved enhancer-like sequence in intron 1 is significantly associated with Hirschsprung disease susceptibility
- Single nucleotide polymorphisms of RET is associated with Hirschsprung disease
- medullary thyroid carcinoma manifested in new RET mutation and RET polymorphism.
- in the presence of RET oncoproteins, both RAI and GAB 1 are tyrosine-phosphorylated, and the stoichiometry of this interaction remarkably increases
- Substantial discrimination between predicted functional classes of RET mutations and disease severity even for a multigenic disease such as Hirschsprung disease.
- Mutations in medullary thyroid cancer and in multiple endocrine neoplasia 2.
- RET/PTC is able to phosphorylate the Y315 residue of PKB, an event that results in maximal activation of PKB for RET/PTC-induced thyroid tumorigenesis.
- determination of mutation specific gene expression profiles in papillary thyroid carcinoma
- C630R mirrors C634R in penetrance and in early age of onset of medullary thyroid carcinoma
- PHOX2A, but not PHOX2B, seems to act directly on the c-RET promoter
- The histone acetylation level was evaluated by the chromatin immunoprecipitation method applied to cells displaying different degrees of endogenous RET expression.
- direct interaction between RET and a broad range of effector molecules that may contribute to tumor pathogenesis
- The RET/PTC1 oncogene activates a proinflammatory program, provide a direct link between a transforming human oncogene, inflammation, and malignant behavior.
- Y1062 is a critical regulator of Ret9 signaling and suggest that Ret51-specific motifs are likely to inhibit the activity of this isoform
- significant association of the S691 allele with medullary thyroid carcinoma
- RET enhancer modulates expression in the enteric nervous system consistent with its proposed role in Hirschsprung disease
- Germline mutation on the RET gene was present in patients with pheochromocytoma or functional paraganglioma.
- Single nucleotide polymorphism in ret is associated with the aggressive growth of pancreatic cancers
- The newly identified RET/N777S germline mutation is a low-penetrant cause of medullary thyroid carcinoma.
- possibility that lower-penetrance RET mutations may contribute to the list of causes of familial pheochromocytomas
- new missense point mutation in exon 5 in familial medullary thyroid carcinoma
- Two Hirschsprung disease-associated haplotypes derive from a single founding locus, extending up to intron 19 and successively rearranged in correspondence with a high recombination rate region located between the proximal and distal end of the RET gene.
- gene expression impairment seems to be at the basis of the association of HSCR disease with several RET polymorphisms, allowing us to define a predisposing haplotype spanning from the promoter to exon 2.
- These results reveal novel roles of key RET-dependent signaling pathways in embryonic kidney development and provide murine models and new insights into the molecular basis for CAKUT.
- Characterization of the R833C substitution suggests that this tyrosine kinase mutation confers a weak activating potential upon RET but introduces an intracellular cysteine which activate RET.
- frequency of RET rearrangements in papillary thyroid carcinoma for the Polish population
- Erk8 has a role as a novel effector of RET/PTC3 and, therefore, RET biological functions
- Mutational screening of RET revealed 9 different mutations, present in 26 of the 114 MEN 2 Spanish patients.
- Gas1 is related to the GDNF alpha receptors and regulates Ret signaling
- evaluation of noncoding sequences at the zebrafish ret locus conserved among teleosts, and at the human RET locus, conserved among mammals
- Mutagenesis analysis revealed that Tyr981 within the intracellular domain of RET was crucial for the interaction with SH2-Bbeta. Morphological evidence showed that SH2-Bbeta and RET colocalized in mesencephalic neurons.
- Medullary thyroid carcinoma as part of multiple endocrine neoplasia type 2 in a family with a mutation in RET proto oncogene.
- strong propensity to self-association in the RET-transmembrane underlies - and may be required for - dimer formation and oncogenic activation of juxtamembrane cysteine mutants of RET
- Some patients with apparently sporadic pheochromacytoma were carrier of mutations in RET proto-oncogene.
- Findings identify RET as a novel substrate of PTPRJ and suggest that PTPRJ expression levels may affect tumor phenotype associated with RET/PTC1 and RET(C634R) mutants.
- Analysis of the RET gene revealed neither linkage nor mutations in Hirschsprung's disease mapping.
- Cell type-specific functions involve a competitive recruitment of different phosphotyrosine binding adaptor molecules by RET that activate selective signaling pathways.
- We show that RA-induced differentiation is mediated by a positive autocrine loop that sustains Ret downstream signaling and depends on glial cell-derived neurotrophic factor expression and release.
- Timing and extent of prophylactic thyroidectomy can be modified by individual RET mutation
- the RET finger protein has a role in estrogen receptor-mediated transcription in tumor cells
- Ret mutations in thyroid tumorigenesis.
- First molecular studies on a complex germline RET mutation lying in the juxtamembrane region of the receptor are reported in medullary thyroid carcinoma
- RET dysfunction has a crucial role and discusses RET as a potential therapeutic target.
- A variant located in the 3' untranslated region of the RET gene, which slows down mRNA decay in patients with Hirschsprung disease.
- These results suggest that RFP is a mediator connecting several MBD proteins and allowing the formation of a more potent transcriptional repressor complex.
- Identification of a heterozygous germ line missense mutation at codon 634 of exon 11 in the RET gene that causes a cysteine to arginine amino acid substitution in a MEN2A patient.
- The molecular basis for HPT has been further elucidated by teh detection of inactivating germline mutations in the CaSR gene in familial hypocalciuric hypercalcemia syndrome and in the RET genes in the familial forms of HPT.
- results indicate a possible association between the presence of lymph node involvement at the time of diagnosis (extent of disease) of medullary thyroid carcinoma and L769L or S836S polymorphism.
- tumor samples from FMTC patients showed strong nuclear staining of phosphorylated ERK1/2 and Ser(727) STAT3; FMTC-RET mutants activate a Ras/ERK1/2/STAT3 Ser(727) pathway, which plays an important role in cell mitogenicity and transformation.
- Copy gain of PDGFB occurs in a subset of tumors showing no evidence of mutated BRAF or rearranged ret, suggesting that copy gain of PDGFB may underlie the increased expression of platelet-derived growth factor described recently in the literature.
- study demonstrated RET amplification in all 3 cases of radiation-associated thyroid cancers(papillary thyroid cancer (PTC) & anaplastic thyroid cancer(ATC) but not in sporadic well-differentiated PTC; RET amplification was observed in all 6 cases of ATCs
- Children of families with RET cysteine mutations may develop early metastatic medullary carcinoma of the thyroid gland.
- the absence of RET alterations in all cases of C-cell hyperplasia
- our results suggest that SPRY2 regulates GDNF-dependent proliferation and differentiation of TGW neuroblastoma cells mediated by RET tyrosine kinase.
- These data highlight the pivotal role of the RET gene in both isolated and syndromic Hirschsprung disease.
- RET, a receptor tyrosine kinase involved with differentiation, was consistently up-regulated throughout the time course of retinoic acid treatment in the majority of neuroblastic tumor cell lines.
- study demonstrates that the interaction between RET and PHOX2B polymorphisms has a substantial impact on risk of Hirschsprung's disease
- prevalence of BRAF mutation and RET/PTC were determined in diffuse sclerosing variant of papillary thyroid carcinoma; RET/PTC1 and RET/PTC3 were found in <50% of the cases investigated
- overexpression of SH2B1beta, by enhancing phosphorylation/activation of RET transducers, potentiates the cellular differentiation and the neoplastic transformation thereby induced, and counteracts the action of RET inhibitors.
- These findings provide evidence for a novel cooperative interaction between VEGFR2 and RET that mediates VEGF-A functions in ureteric bud cells.
- primary hyperparathyroidism in RET 630 mutations might be associated with lower penetrance of primary hyperparthyoidism and pheochromocytoma
- five RET sequence variants were detected in Hirschprung disease patients, including G15165A in exon 11, G20692A in exon 15, A18919G, T18888G, and a frameshift mutation 18974insG in exon 13
- RET proto-oncogene mutations were restricted to codon 634 and 918 in Chinese families with MEN2A and MEN2B.
- A heterozygous M918T mutation of the RET proto-oncogene was found in MEN 2B patients.
- oncogenic precursor of RET(MEN 2B) is phosphorylated, interacts with adapter proteins and induces downstream signalling from the ER.
- a change in the spectrum of mutations detected in the RET proto-oncogene in patients with hereditary MTC from the 'classical' mutation at codon 634 in exon 11 (level 2) to more cases with mutations in the exons 13-15 (level 1) and less aggressive disease
- Patients harboring Y791F mutation may be considered at risk in an age earlier than 20 years and speculate that L769L variant of RET may be related to the early age of onset.
- The reserachers found RET mutations common in an Iranian population, and these mutations are associated with the development of medullary thyroid carcinoma.
- A fusion product between exon 11 of HOOK3 and exon 12 of RET gene was identified by 5'RACE, and the presence of chimeric HOOK3-RET protein of 88 kDa was detected by western blot analysis with an anti-RET antibody.
- inhibition of RET is not impaired by mutation of the Val(804) gatekeeper residue, so MEN2 tumors may be less susceptible to acquired Sorafenib resistance
- BRAF(V600E) mutation detected on fine-needle aspiration biopsy specimens, more than RET/PTC rearrangements, is highly specific for papillary thyroid carcinoma.
- No RET rearrangement is associated with the papillary thyroid carcinomas
- In the medulla oblongata, labekke nerve fibers, punctate structures, abd cell bodies occured in the caudate and interpolar parts of the spinal trigeminal nucleus.
- We unexpectedly discovered a germline RET mutation in 35 of 481 (7.3%) apparently sporadic medullary thyroid carcinoma patients
- expression of RET, nuclearRAS, and ERK proteins is greatly enhanced in papillary thyroid carcinoma cells and Hashimoto's thyroiditis oxyphil cells.
- review summarizes how the different domains of the RET protein contribute to its normal function and how mutations in these domains affect the function of the receptor[Review]
- This report reviews the RET involvement in the etiology of multiple endocrine neoplasia (MEN) 2 and medullary thyroid cancer (MTC) and updates the therapeutic approach in preclinical and clinical studies.
- A break-apart fluorescence in situ hybridization (FISH) assay should be able to detect translocations involving the RET gene in a papillary thyroid carcinoma cell line.
- occurrence and the type of germline mutations in the RET gene in patients with medullary thyroid carcinoma.
- The penetrance of pheochromocytoma varies between multiple endocrine neoplasia 2A RET codon mutations
- the presence of a somatic RET mutation correlates with a worse outcome of MTC patients, not only for the highest probability to have persistence of the disease, but also for a lower survival rate in a long-term follow up.
- Child with hirschsprung disease and Wilms tumor showed mutations in the RET gene.
- an important function for FRS2 is to concentrate RET in membrane foci, leading to an engagement of specific signaling complexes localized in these membrane domains
- GDNF, NTN, GFRalpha-1, GFRalpha-2, and c-Ret proteins are differentially expressed in the different stages of hair follicle cycle. GFRalpha-mediated signaling involves c-Ret and may play a role in human HF biology.
- frequency of the occurrence of BRAF mutation and/or RET/PTC in H4-PTEN positive tumors was extremely high (75%) in papillary thyroid carcinoma
- Renal aplasia in humans is associated with RET mutations.
- study demonstrates that the Ret Gly691Ser mutation is associated with primary vesicoureteral reflux and may be one of the genetic causes of this condition in the French-Canadian population in Quebec
- A statistically significant correlation between the presence of RET somatic mutations with more advanced pathological neoplasm stages was observed in sporadic medullary thyroid carcinomas.
- TrkB receptor promotes Ret phosphorylation; blocking either TrkB or Ret by small interfering RNA causes a failure in NB biochemical and morphological differentiation.
- uncommon coexistence of a germline mutation in two suppressor genes, RET and CDKN2A in multiple endocrine neoplasia 2a
- oncogenic RET and loss of p18 cooperate in the multistep tumorigenesis of medullary thyroid carcinoma
- a beta-catenin-RET kinase pathway is a critical contributor to the development and metastasis of thyroid carcinoma
- Clinical and in vitro findings indicate that the transmembrane RET S649L mutation is associated with late-onset non-aggressive disease.
- These results suggest that engagement of different adaptor proteins by Ret results in very different downstream signaling and functions within neurons and that Dok recruitment leads to a rapid receptor relocation and formation of microspikes.
- Differential membrane compartmentalization of RET by PTB-adaptor engagement is reported.
- Oncogenic RET mutations may, however, vary between specific population groups. RET analysis in MEN has revolutionized the management of children of MEN2 and allowed surgical prediction and prophylaxis to take place.
- No significan correlation between mutations in this protein and papillary thyroid cancer in Turkey.
- Data show that the increased phosphorylation of tyrosine 1062 of the Ret receptor tyrosine kinase was induced by GDNF. GDNF signal through a molecular complex and the Ret receptor tyrosine kinase.
- The RET proto-oncogene has become the target for molecularly designed drug therapy. Tyrosine kinase inhibitors targeting activated RET are currently in clinical trials for the treatment of patients with MTC.
- Data show that enteric neuron survival is sensitive to RET dosage, and cell death is potentially involved in the etiology of Hirschsprung disease.
- the data support a model in which RET and PHOX2B contribute to the combined phenotype in congenital central hypoventilation syndrome combined with Hirschsprung disease
- the Ret receptor tyrosine kinase pathway functionally interacts with the ERalpha pathway in breast cancer
- The mechanism of activation of downstream signal transduction pathways by RET oncoproteins.
- The majority of medullary thyroid cancers are sporadic, but 20% of cases are a result of a germline mutation in the ret proto-oncogene.
- EGFR contributes to RET kinase activation, signaling, and growth stimulation and may therefore be an attractive therapeutic target in RET-induced neoplasms
- Non-coding mutations in RET have important roles in the development of Hirschsprung's disease.
- The Cys515Ser mutation in Ret exon 8 adds to cysteine substitution groups that have been described in association with medullary thyroid carcinoma.
- Results describe the relationship between overexpression of glial cell-derived neurotrophic factor and its RET receptor with progression and prognosis of human pancreatic cancer.
- The expression of the RET gene showed an increased segmenting from the aganglionic segment to the normal segment.
- Sorafenib potently inhibits papillary thyroid carcinomas harboring RET/PTC1 rearrangement
- RET germ-line mutations are associated with medullary thyroid carcinomas in medullary thyroid carcinoma.
- Importance of candidate tumor suppressor genes together with RET alterations in medullary thyroid carcinoma.
- RET gene mutations in 2 of 15 patients with Hirschsprung's disease in Taiwan. The Y146N mutation we identified was novel.
- Germ line mutation in RET is associated with multiple endocrine neoplasia type 2A.
- In this two-family review the Gly533Cys point mutation of the RET gene seems to be related to multiple endocrine neoplasia type 2A (MEN2A) and possibly to a milder phenotype of the syndrome.
- a variant of the human RET gene increases the risk for aberrant mRNA splicing and is associated with a reduction (approximately 10%) of newborn kidney volume and an increase (approximately 9%) in umbilical cord cystatin C.
- analysis of how GDNF.GFR alpha 1 can mediate cell adhesion and how heparin might inhibit GDNF signaling through RET
- Melanoma-specific memory T cells are functionally active in Ret transgenic mice without macroscopic tumors.
- analysis of how RET protein kinase is inhibited by beta-carbolin-1-ones
- Ret/ptc1 cross talks with Met at transcriptional and signaling levels and promotes beta-catenin transcriptional activity to drive thyrocyte neoplastic transformation.
- report of a family with hereditary head and neck paraganglioma with metastatic dissemination in the liver and the spine; evidence supports the absence of mutations in SDH, RET and VHL genes
- In conclusion, Multiplex Ligation-dependent Probe Amplification assessment of rearrangements in the RET proto-oncogene and in 3 other associated genes, ZEB2, EDN3 and GDNF did not show any variants in 80 sporadic Hirschsprung disease patients.
- molecular mechanism of activation and the functional role of cancer mutations in altering protein kinase structure, dynamics, and stability.