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Validated All-in-One™ qPCR Primer for FLT3(NM_004119.2) Search again
Product ID:
HQP005890
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CD135, FLK-2, FLK2, STK1
Gene Description:
fms related receptor tyrosine kinase 3
Target Gene Accession:
NM_004119.2(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
This gene encodes a class III receptor tyrosine kinase that regulates hematopoiesis. The receptor consists of an extracellular domain composed of five immunoglobulin-like domains, one transmembrane region, and a cytoplasmic kinase domain split into two parts by a kinase-insert domain. The receptor is activated by binding of the fms-related tyrosine kinase 3 ligand to the extracellular domain, which induces homodimer formation in the plasma membrane leading to autophosphorylation of the receptor. The activated receptor kinase subsequently phosphorylates and activates multiple cytoplasmic effector molecules in pathways involved in apoptosis, proliferation, and differentiation of hematopoietic cells in bone marrow. Mutations that result in the constitutive activation of this receptor result in acute myeloid leukemia and acute lymphoblastic leukemia. [provided by RefSeq].
Gene References into function
- First report of D835X mutations in human. Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies.
- Mechanism of constitutive activation of FLT3 with internal tandem duplication in the juxtamembrane domain
- Flt3/Flk-2-ligand in synergy with thrombopoietin may slow down megakaryocyte development by causing increased proliferation of megakaryocyte progenitor cells.
- Analysis of FLT3-activating mutations in patients with acute myelogenous leukemia: association with FAB subtypes and identification of subgroups with poor prognosis.
- induces acute promyelocytic leukemia in a mouse model
- Analysis of FLT3 length mutations in 1003 patients with acute myeloid leukemia
- duplicated in relapsed acute myeloid leukemia
- mutations occur in paired presentation and relapse samples from patients with acute myeloid leukemia
- FLT3 with internal tandem duplication mutations from myeloid leukemia patients blocks myeloid differentiation when transfected into 32Dc13 cells.
- 767 of 6586 genes differed in expression between FLT3-WT- and FLT-ITD(internal tandem duplication)-expressing cell lines. ITD mutations of Flt3 activate transcriptional programs that partially mimic IL-3 activity.
- Internal tandem duplication of the Flt3 gene appearing or altering at time of AML relapse suggests Flt3-gene abnormalities are very important in the pathogenesis of chemotherapy-resistant AML
- The striking difference in flt3 and c-kit expression on hematopoietic stem cells translated into a corresponding difference in flt3 and c-kit function because FL was more efficient than SCF at supporting the survival of HSCs
- Intracellular signaling initiated by Flt3 ligation modulates the functional phenotype for native human AML blasts both with and without genetic Flt3 abnormalities.
- REVIEW ARTICLE. FLT3 mutations that lead to constitutive receptor activation and confer a poor prognosis in AML
- FLT3/ITD is less common in pediatric than in adult acute myeloid leukemia and FLT3/ITD is a strong and independent adverse prognostic factor, and high ratios between mutant and WT-FLT3 further compromise prognosis.
- antiapoptotic pathways from FLT3 with internal tandem duplication are more divergent than those from WtFLT3
- Mutations in the FLT3 gene are common in AML, including tandem repeats or a mutation in the kinase domain.
- No significant correlation was found between FLT3 mutations and high levels of MDR1 in acute myeloid leukemia.
- REVIEW: The role of FLT3 mutations in APL and other AML
- wtFLT3 is often constitutively activated by FLT3 ligand in AML and thus, like its mutated form, might contribute to the altered signaling that characterizes leukemogenesis.
- FLT3-D835/I836 mutations are one of the second genetic events in infant ALL with MLL rearrangements or pediatric ALL with hyperdiploidy
- reduced AML1 activities predispose cells to the acquisition of the activating FLT3 mutation as a secondary event leading to full transformation in acute myeloblastic leukemia M0
- distinct activating FLT3-TKD mutations at position D835 mediate primary resistance to FLT3 PTK inhibitors in FLT3-transformed cell lines
- FLT3 mutations are associated with molecular lesions in acute myeloid leukemias
- Phosphorylation is inhibited by SU11248 in acute myeloid leukemia.
- search for the presence of FLT3 mutations in leukemic blasts from 71 patients with childhood acute lymphoblastic leukemia discovered three novel in-frame deletions within a 7-amino acid region of the receptor juxtamembrane domain.
- Acquisition of FLT3 mutations is frequently associated with progression of myelodysplastic syndrome to acute myeloid leukemia
- FLT3 analysis shows the autoinhibitory conformation of its complete juxtamembrane domain
- FLT3 Asp(835) mutations may have a role in relapse of acute myeloid leukemia
- FLT3 can negatively regulate Foxo transcription factors, thereby promoting cell survival and proliferation.
- Mutations of Flt3 may disrupt transcriptional repressor function resulting in aberrant gene regulation and abnormal leukemia cell growth.
- Activating mutations in the FLT3 RTK gene were found in each of 3 CD117/KIT(+) cases that were analyzed, but not in 52 other adult T-acute lymphoblastic leukemia
- CXCR-4 expression was significantly higher in fetal liver tyrosine kinase-3 (Flt3)/internal tandem duplication (ITD) acute myeloid leukemia
- Internal tandem duplication of the juxtamembrane domain or by activating point mutations in the second tyrosine kinase domain in FLT3 are associated with leukocytosis and the monocytic FAB subtypes M4 and M5.
- Flt3 mutations identify patients at high risk of relapse
- FLT3/internal tandem duplication(ITD) mutations confer a particularly poor prognosis in pediatric acute myelogenous leukemia patients
- high frequency of FLT3 mutations in adult acute myelocytic leukemia without recurrent cytogenetic translocations.
- FLT3 autoinhibited structure showed that N841 is the key residue in a hydrogen-bonding network that likely stabilizes the activation loop
- Wild-type Flt3-overexpressing CD34+ cells exposed to high levels of its physiologic ligand did not produce early cobblestone areas
- FLT3 has roles in different signal transduction pathways that control proliferation, survival and other processes in hematopoietic cells [review]
- The loss of a clone with a mutation in the FLT3 gene at relapse did not improve the prognosis.
- Inspection of the FLT3 structure revealed that Y842 is the key residue in regulating the switch from the closed to the open (= active) conformation of the FLT3 activation loop
- mutations of specific residues located in the activation loop (D835X and 836-deletion in Flt-3; D816V in c-Kit) as well as a 6-base pair (6-bp) insertion at residue 840 in Flt-3 operate in a similar way
- transformation of TF-1 cells with FLT3/ITD mutations suppressed the activity of SHP-1 by approximately 3-fold
- FLT3 mutations cause autoactivation and uncontrolled signaling in leukemia [review]
- The FLT3 is widely expressed in AML and some cases of acute lymphocytic leukemia.
- The FLT3 gene, partial tandem duplication of the MLL gene, mutations of the CEBPA gene, and overexpression of the BAALC gene-have been found to predict outcome in patients with AML and normal cytogenetics.
- Potential impact of Flt3 based residual cancer status not only after but also prior to allogeneic peripheral blood cell transplantation.
- Flt3-ITD and Wnt-dependent signaling pathways synergize in myeloid transformation
- FLT3 gene expression might lead to the identification of further pathogenetic relevant candidate genes particularly in AML with normal karyotype.
- MLL and FLT3 gene duplications could have roles in myeloid malignancies
- Flt3-ITD and Flt3-TKD mutations display differences in their signaling properties
- Circulating FLT-3 levels didn't increase in early neonatal life
- FLT-3 is primarily expressed by hematopoietic cells & plays an important role in hematopoiesis. FLT-3 is also expressed in the majority of acute leukemias, in which the presence of FLT-3 activating mutations is associated with poor prognosis [review]
- involvement of Src kinases in Flt3 signaling, with activation of Lyn by constitutively active Flt3 mutants as well as ligand-stimulated wild-type receptor; cell proliferation resulting from mutant Flt3 expression did depend on the activity of Src kinases
- Internal tandem duplication mutations of the FLT3 gene are present in leukemia stem cells.
- The maturation of wild-type FLT-3 is impaired by general protein-tyrosine phosphatases inhibition or by suppression of endogenous PTP1B.
- Determination of minimal residual disease based on patient specific Flt3 internal tandem duplication and internal tandem triplication mutation in acute myeloid leukemia.
- The Activating mutations or over-expression of the Flt3 is prevalent in acute myeloblastic leukemia (AML), associated with activation of NF-kappaB signaling pathways.
- FLT3 internal tandem duplication mutation is capable of inducing myeloproliferative as well as lymphoid disease
- FLT3 is a therapeutic target and inhibition of FLT3 tyrosine kinase activity may provide a new approach in the treatment of leukemia carrying these mutations. (review)
- Langerhans cells are derived mainly from myeloid progenitors and are dependent on Flt3-ligand for their development.
- Our data suggest that the FLT3 D324N variant might be associated with a predisposition to different subtypes of leukemia.
- confirmation of FLT3 mutations in pediatric T-cell acute lymphoblastic leukemias
- FLT3 internal tandem duplications in the juxtamembrane domain are found in approximately 25% of acute myeloid leukemia patients, ranging in size from 3 to hundreds of nucleotides, and may have prognostic significance.
- characterized a new class of activating point mutations that cluster in a 16-amino acid stretch of the juxtamembrane domain of FLT3
- methods for detecting internal tandem duplication and D835 missense mutations in the FLT3 gene in acute myeloid leukemia.
- Flt3L reconstitutes a crucial afferent component of the immune response
- FLT3 mutations were significantly associated with a shorter EFS and survival (P<0.0001 and P=0.0002) owing to an excess of early events.
- Gain of FLT3 internal tandem duplication(ITD) may suggest oligoclonality with selective outgrowth of the FLT3/ITD-positive clone, whereas losses may reflect ITDs in the more mature leukemic cells rather than in the leukemic stem cell
- Recruitment of SHP2 to specific sites of autophosphorylation contributes to FLT3-mediated Erk activation and proliferation.
- Using FLT3 internal tandem duplication (FLT3/ITD) as a molecular marker, we tested the hypothesis that clinical outcome in AML correlates with disease involvement of CD34(+)/CD33(-) precursors.
- synergism between NUP98-HOX and wt-Flt3 is the result of the ability of Flt3 to increase proliferation of myeloid progenitors blocked in differentiation by NUP98-HOX fusions, revealing a direct role for wt-Flt3 in the pathobiology of AML.
- four novel point mutations described; observation indicates that the point mutations occur simultaneously with the ITD mutations in AML
- FLT3 mutations in acute myeloid leukemia can involve novel regions of the amino terminal (TK1)
- no correlation between size of duplicated sequences of FLT3 and disease outcome in acute myeloid leukemia patients
- the prognostic relevance of foetal liver tyrosine kinase 3 (FLT3) mutations in 73 patients with acute myeloid leukaemia
- FLT3 mutation is associated with M1/M2 AML samples
- FLT3 mutations were associated with higher leukemic burdens and early deaths
- Bcl-2 inhibition might therefore improve the efficacy of existing acute myeloid leukemia therapies by inactivating this suppression of wild-type p53 activity
- inhibition of ITD/Flt3 activity did not prevent the phosphorylation of ERK, STAT5 or Akt in some primary AML cells. In parallel, in these cells, Flt3 and ERK or Akt cooperate to regulate cell survival
- PDGFRbeta and FLT3 mutants are inhibited by sorafenib
- FLT3/ITD (internal tandem duplication)specifically associates with Lyn, phosphorylating Lyn in vivo. FLT3/ITD receptors bind Lyn with more affinity than wild-type in transfected mouse cells, relative to the degree of receptor tyrosyl phosphorylation.
- Transgenic mice expressing constitutively activated human FLT3 develop myeloproliferative diseases with a long latency.
- stem-cell transplantation in first remiaaion seem to be warranted to compensate for negative prognostic impact of FLT3/ITD
- Molecular mechanism of transformation by FLT3-internal tandem duplicationsis are important for the leukemic potential of FLT3.
- FLT3 has a role in proliferation of normal hematopoietic progenitor cells
- Activating mutations of FLT3 tyrosine kinase is associated with acute myeloid leukemia
- FLT3 overexpression is associated with acute myeloid leukemia
- Both ionizing radiation and daunorubicin treatment resulted in concerted protein modulations of Mcl-1, Hdm2 and Flt3.
- an association of FLT3/ITD with the adverse outcome in AML patients treated with standard induction chemotherapy.
- highlights the role of FLT3 in hematopoiesis, and how when activated, it may play a role in the development of acute myeloid or acute lymphoblastic leukemia
- FLT3 internal tandem duplications may increase potential for cell proliferation to produce a leukaemic population
- FLT3 activating mutations were significantly associated with a bcr3 PML-RARalpha isoform (p=0.012) and a delay in achieving a molecular remission
- These results suggest that FLT3 polymorphisms play a role in determination of BMD and subsequent fractures in postmenopausal women.
- Trisomy 13 patients with a RUNX1 mutation showed a 4-fold higher expression of FLT3 mRNA compared to controls.
- in hematopoietic cells, the JM region of fems-like tyrosine kinase 3(FLT3)is phosphorylated by hematopoietic cell kinase (hct)
- TSC-22 is a potential tumor suppressor that is upregulated by Flt3-D835V but not Flt3-ITD
- AML patients with FLT3-ITD, but not D835Mt, showed a poor prognosis. AML patients with MLL-PTD were also correlated with poor prognosis in this study.
- Activated FLT3 cooperates with MLL-AF9 to accelerate onset of acute myelogenous leukemia
- FLT3 activation induces beta-catenin tyrosine phosphorylation and nuclear localization, suggesting a mechanism for the association of FLT3 activation and beta-catenin oncogeneic signaling in AML.
- conclude that constitutively activated FLT3 as a result of increased expression may contribute to the dismal prognosis of MLL-rearranged infant acute lymphoblastic leukemia
- phosphorylated STAT5 could be the most meaningful test for rapidly identifying patients who may respond to flt3 or other tyrosine kinase inhibitors
- Frequently mutated in high hyperdiploid childhood acute lymphoblastic leukemia.
- Identified FLT3 internal tandem duplication mutations in a subset of human chronic myelonomocytic leukemia.
- may lead to development of novel therapies that improve clinical outcome of cytogenetically normal acute myeloid leukemia patients with FLT3-TKD
- In the present quite limited series, FLT3 mutations do not seem to have a major impact on global gene expression pattern in childhood acute leukemias.
- There was a highly significant trend for worsening in relapse risk (RR) and overall survival (OS) with increasing FLT3/ITD (internal tandem duplication) mutant level.
- The mutational status of the FLT3 tyrosine kinase domain (FLT3-TLD) in 3082 patients with newly diagnosed acute myeloid leukemia, was characterized.
- correlation of PTPN11 mutations with NPM1 mutations and FLT3/ITD among adult AML patients
- Activating mutations of FLT3 is associated with acute myelogenous leukemia
- In 51 clinical JMML samples,activating mutations were screened, FLT3 and FLT3L mRNA levels were assessed. No evidence for constitutive activation of FLT3/FLT3L was found in JMML
- screened the entire FLT3 coding sequence in MLL rearranged and hyperdiploid ALL cases for yet unidentified additional genetic alterations using denaturing D-HPLC; a small minority of samples, 7% and 10% respectively, carried genetic alterations.
- a large series of proteins is differently expressed in primary AML blasts harboring FLT3-ITD mutations.
- study shows that the frequency of FLT3/ITD mutation in myelodysplastic syndromes (MDS)is low and is not always associated with high risk MDS
- A high-throughput platform was used to interrogate the entire FLT3 coding sequence in Leukemia, Monocytic, Acute patients without known FLT3 mutations and the consequences of each candidate leukemogenic allele was experimentally tested .
- The FLT3 inhibitor PKC412 exerts differential cell cycle effects on leukemic cells depending on the presence of FLT3 mutations.
- Elderly patients (range 60-85 yr) with acute myeloid leukemia carrying Flt3 internal tandem duplications (ITD) have a significant worse overall survival compared to Flt3-ITD wildtype patients.
- IL1R2 was greatly decreased with future rejection and FLT3, ITGAM, and PDCD1 showed borderline changes in future cardiac rejections.
- Potentiation of antileukemic therapies by the dual PI3K/PDK-1 inhibitor, BAG956: effects on BCR-ABL- and mutant FLT3-expressing cells.
- There was a nonsignificant trend for FLT3/ITD mutation to be associated with a poorer predicted overall survival (OS) probability in this population
- aggressiveness of the disease and poor prognosis of AML patients with FLT3/ITD mutations could be the result of increased genomic instability
- The localization of FLT3, a subclass III receptor tyrosine kinase frequently mutated in leukemia, is investigated.
- Physical characteristics including the length of FLT3/ITD may influence FLT3 activation state by altering its structure and may impact response to therapy
- gene-expression patterns correlated with FLT3-ITD mutation and evaluation of the utility of a FLT3 signature for prognostication.
- close association of aberrant CD7 expression and FLT3/ITD mutation in the myeloblasts of FLT3/ITD+ acute myeloid leukemia suggests that FLT3/ITD- mediated leukemic transformation occurs in the more early stage of myeloid progenitor cells
- analysed the frequency and prognostic impact of ITD and D835 mutations in a cohort of 120 consecutive elderly AML patien
- FLT3 mutation in acute myeloid leukemia confers a poorer prognosis in disease-free survival and overall survivalan even with a concomitant nucleophosmin1 (NMP1) mutation, which is normally a good prognostic factor.
- FLT3 signaling might play an important role in cell survival, especially at stem and progenitor cells that are critical cellular targets for acute myelogenous leukemia transformation
- FLT3 internal tandem repeat is associated with a high probability of evolution of myelodysplastic syndrome to acute myeloid leukemia
- This protein, which is mutated in majority of cases of acute myeloid leukemia, is used as an example or a method which may apply to the quantitation of several other proteins without the need for intact cells.
- NPM1 mutants coexisted mainly with FLT3 mutants
- These results suggest that Flt3 inhibitors might exert an anti-neoplastic effect in high-risk myelodysplastic syndrome and acute myeloid leukemia through inhibition of NFkappaB.
- In a series of human AMKL samples from both Down syndrome and non-Down syndrome patients, mutations were identified within KIT, FLT3, JAK2, JAK3, and MPL genes, with a higher frequency in DS than in non-DS patients.
- FLT3 and its ligand regulate proliferation of hematopoietic progenitor cells in an autocrine and/or paracrine manner.
- Association between overexpression of FLT3 and a positive FLT3/ITD mutation and a poor prognosis and negative clinical presentation in acute leukemia.
- analysis of low frequency and variability of FLT3 mutations in Korean patients with acute myeloid leukemia
- KIT and FLT3 mutations preferentially exist in distinct clinical and genetic acute myeloid leukemia subtypes, reflecting unique leukemogenetic mechanisms.
- Combined mobilization and stimulation of tumor-infiltrating dendritic cells and natural killer cells with FLT3 ligand and IL18 in vivo induces systemic antitumor immunity.
- a significant proportion of acute promyelocytic leukemia with t(15;17) patients (56%) showed additional karyotype alterations and/or FLT3/ITD or D835Y mutation.