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Validated All-in-One™ qPCR Primer for NTRK2(NM_006180.3) Search again
Product ID:
HQP011945
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
DEE58, EIEE58, GP145-TrkB, OBHD, TRKB, trk-B
Gene Description:
neurotrophic receptor tyrosine kinase 2
Target Gene Accession:
NM_006180.3(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.
Summary
This gene encodes a member of the neurotrophic tyrosine receptor kinase (NTRK) family. This kinase is a membrane-bound receptor that, upon neurotrophin binding, phosphorylates itself and members of the MAPK pathway. Signalling through this kinase leads to cell differentiation. Mutations in this gene have been associated with obesity and mood disorders. Alternate transcriptional splice variants encoding different isoforms have been found for this gene. [provided by RefSeq].
Gene References into function
- analysis of TrkB gene reveals novel gene length and splicing mechanism
- Alterations in trkB mRNA in the human prefrontal cortex throughout the lifespan.
- discrete domain of the TrkB receptor defines the binding sites for BDNF and NT-4
- This review discusses the importance of TrkB/brain-derived neurotrophic factor signaling pathway interactions in memory processes.
- expressed in human neuroblastoma cells in response to retinoic acid
- Messenger RNA levels of BDNF and trk B were significantly reduced, independently and as a ratio to neuron-specific enolase, in both prefrontal cortex and hippocampus in suicide subjects, as compared with those in control subjects.
- Observed immunohistochemical differences in TrkB between schizophrenic and normal cases may indicate the existence of TrkB dysfunction in schizophrenic brain, and this dysfunction may be one of the factors involved in the pathogenesis of schizophrenia.
- Results suggest that basic helix-loop-helix proteins provide a direct transcriptional link between a cell cycle inhibitor, p21(Cip1), and a neurotrophic receptor, Trk.
- An 8-year-old male with a complex developmental syndrome and severe obesity was heterozygous for a de novo missense mutation resulting in a Y722C substitution in the neurotrophin receptor TrkB.
- upregulation of genes involved in neoplasm invasiveness or therapy resistance
- We investigated the involvement of signaling mediated by brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase TrkB in producing the altered GABA-related gene expression in schizophrenia.
- MM cells express TrkB, and respond to BDNF by activating MAPK and PI3K/Akt signaling cascades
- Contribution of NTRK2 to the genetic susceptibility of eating disorders, mainly anorexia nervosa, harm avoidance and body mass index.
- The neurotrophin receptor TrkB cooperates with c-Met in enhancing neuroblastoma invasiveness
- Results showed that TrkB receptor was identified in oocytes and GCs and the transcripts of all forms of TrkB receptor were identified in the samples.
- TRKb is likely to play roles not only in early growth but also in maintenance of neurons throughout life.
- These results strongly suggest that NTRK2 is a susceptibility gene for ND. These findings imply that NTRK2 plays a role in the etiology of ND and represents an important biological candidate for further investigation.
- Light and electron microscopy immunohistochemistry showed that tonsillar samples were positive for TrkB.
- Human lung adenocarcinomas express TrkA and TrkB, but not TrkC; A549 cells, express mRNA transcripts encoding nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), TrkA, TrkB, and p75, and high protein levels of TrkA and TrkB.
- EGFR and TrkB crosstalk each other in response to EGF and BDNF, leading to cell survival pathway activation in ovarian cancer cells.
- TrkB may be a mediator as well as a marker of carcinogenesis and metastasis.
- Support role for NTRK2 gene in addiction in Caucasian population with antisocial alcohol dependence.
- Decreased TrkB transgene expression or retina-specific deletion of TrkB, the cognate receptor for BDNF, retards the laminar refinement of ganglion cell dendrites.
- TrkB kinase activity is required and, unexpectedly, also sufficient for anoikis suppression, tumor formation, and experimental metastasis
- Thus, these results do not support a significant role for TrkB sequence variation in the etiology of schizophrenia.
- TrkB expression may be greater in women with endometriosis compared to women without endometriosis.
- We used a linkage disequilibrium (LD)-mapping approach to investigate the role that BDNF and its specific receptor neurotrophic tyrosine kinase receptor type 2 (NTRK2) may play in increasing susceptibility to OCD.
- the BDNF/TrkB signaling pathway could be involved, at least in part, in multiple myeloma-induced angiogenesis
- results suggest that NTRK2 may be a genetic susceptibility gene contributing to Alzheimer disease pathology
- in astrocytomas, Trk receptors (TrkA, TrkB, TrkC) expression, but not p75NTR may promote tumor growth independently of grade
- NTRK2 gene that encodes the BDNF receptor, TRKB, was overexpressed in MeCP2 deficient human and mouse brains either directly or as an attempt to compensate for BDNF deficiency
- TrkB might mediate anoikis suppression by activating the PI3K-AKT pathway in ovarian cancer cells.
- Review provides future perspective on BDNF/TrkB signaling as a novel molecular target to correct the pathogenesis of schizophrenia and improve its long-term clinical outcome by treatments with conventional and adjunctive drugs.
- TrkB receptor promotes Ret phosphorylation; blocking either TrkB or Ret by small interfering RNA causes a failure in NB biochemical and morphological differentiation.
- somatic mutations in the tyrosine kinase domain of NTRK2 gene are frequent in large cell neuroendocrine carcinomas. Such mutational events could represent an important step in the cancerogenesis of these tumors
- A potential role of all neurotrophins, through their different receptors, in pituitary functions.
- Retinal brain-derived neurotrophic factor BDNF/TrkB signaling has a primary role in the development of inner retinal neuronal circuits in conditional knockout mice. This action is not a secondary effect due to loss of visual signaling in the outer retina
- The impact of Trk receptor expression on nonhomologous end joining-mediated DNA double-strand breaks repair, was analyzed.
- Expression of Trk-A and Trk-B by cells of the nondegenerate and degenerate intervertebral disc suggests an autocrine role for neurotrophins in regulation of disc cell biology.
- A reduction of TrkB.T1 expression in the frontal cortex of a subpopulation of suicide completers is associated with the methylation state of the promoter region.