TRKB, Active Human Recombinant Protein
- Known as:
- TRKB, Active Human Recombinant Protein
- Catalog number:
- 40281
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- Biotech support group
- Gene target:
- TRKB Active Human Recombinant Protein
Related genes to: TRKB, Active Human Recombinant Protein
- Gene:
- NTRK2 NIH gene
- Name:
- neurotrophic receptor tyrosine kinase 2
- Previous symbol:
- -
- Synonyms:
- TRKB
- Chromosome:
- 9q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-18
- Date modifiied:
- 2018-07-09
Related products to: TRKB, Active Human Recombinant Protein
Related articles to: TRKB, Active Human Recombinant Protein
- , , and gene fusions are rare oncogenic driver alterations found in diverse tumor types of adults and children. They are clinically important biomarkers as tumors harboring these genomic alterations have high response rates to targeted therapy. Routine testing for fusions and treatment with TRK inhibitors has been recommended in multiple tumor types; however, differences between testing technologies used for detecting fusions can result in variable likelihoods of identification. - Source: PubMed
Publication date: 2025/05/02
Wallen Zachary DTierno MarniSchnettler EricaRoos AlisonGreen MichelleAmoah KobinaPrevis Rebecca AHastings StephaniePabla SarabjotJensen Taylor JCaveney BrianEisenberg MarciaSathyan PratheeshRamkissoon Shakti HSeverson Eric A - Circular RNAs (circRNAs) have been reported to function critical roles in the pathogenesis and progression of nasopharyngeal carcinoma (NPC). The role of circNTRK2 (circbase ID: hsa_circ_0139142) remains dimness in this disease. This study aimed to investigate the effects and underlying mechanism of circNTRK2 in NPC. GSE143797 was downloaded from the Gene Expression Omnibus (GEO) database, and differently expressed circRNAs were analyzed by the GEO2R method. CircNTRK2 expression was confirmed in human NPC tumor tissues and cell lines by real-time PCR. Loss-of-function studies were used to explore the influence of circNTRK2 on the proliferation, invasion, apoptosis, and epithelial-mesenchymal transition (EMT) of NPC cells. Then, bioinformatic analysis, luciferase reporter assay, biotinylated miRNA pull-down assay, real-time PCR, and Western blotting were applied to clarify the detailed mechanism. We found that circNTRK2 was highly expressed in NPC tissues and cells. Silencing of circNTRK2 inhibited proliferation, invasion and EMT, but facilitated apoptosis of NPC cells in vitro. Also, downregulation of circNTRK2 suppressed tumor growth in a xenograft mouse model. CircNTRK2 directly targeted and negatively mediated miR-384 expression. SOX4 was a target gene of miR-384 in NPC. Both miR-384 inhibitor and SOX4 upregulation could reverse the effects of circNTRK2 knockdown on the proliferation, invasion, EMT, and apoptosis of NPC cells. Whereas miR-384 mimics and SOX4 knockdown abrogated the influences of circNTRK2 upregulation on NPC cells. In conclusion, circNTRK2 promoted NPC progression via sponging miR-384 and inhibiting miR-384 activity, leading to the upregulation of SOX4. This study indicated that circNTRK2 might be a potential target for the treatment of NPC. - Source: PubMed
Publication date: 2025/05/16
Kang LinLiu YangZheng GuonaHu ZhijuanYang Fan - - Source: PubMed
Publication date: 2025/05/13
Osonoi KasumiSawada AkinariMaekawa YukiYamaguchi MariYamada ShingoMatsuyama KazuhiroRochman MarkRothenberg Marc EHan XiaoboMatsuda NaokiSuzuki IkuroTanaka FumioFujiwara YasuhiroShoda Tetsuo - Precision medicine programs like the Zero Childhood Cancer Program perform comprehensive molecular analysis of patient tumors, enabling detection of novel structural variants that may be cryptic to standard techniques. Identification of these variants can impact individual patient treatment, and beyond this establish new mechanisms of oncogenic activation. We have identified a novel internal tandem duplication (ITD) in the receptor tyrosine kinase (RTK), NTRK2, in a patient with FOXR2-activated CNS neuroblastoma. The ITD spans exons 10-13 of NTRK2 encoding the transmembrane domain. NTRK2 ITD is transforming and sensitive to TRK inhibition. In silico structural predictions suggested the duplication of an alpha-helix region and juxtaposed tyrosine residues that play a role in facilitating autophosphorylation. Consistent with this, mutation of these residues inhibited cellular transformation. This is the first report of an ITD spanning the transmembrane domain of an RTK, characterizing an additional mechanism by which RTKs are activated in cancer. - Source: PubMed
Publication date: 2025/05/10
Brown Lauren MTax GaborAcera Mateos Pablode Weck AntoineForesto SteveRobertson ThomasJalud FatimahAjuyah PamelaBarahona PauletteMao JieDolman M Emmy MWong MarieMayoh ChelseaCowley Mark JLau Loretta M SSadras TeresaEkert Paul G - Repeated ketamine treatment to maintain a rapid antidepressant effect can lead to side effects over time, highlighting an unmet clinical need for sustaining this drug's antidepressant action from a single administration. Ketamine-induced synaptic potentiation at CA3-CA1 synapses has been proposed to be a key synaptic substrate for antidepressant action. Here, we found that ketamine-induced CA3-CA1 synaptic potentiation could be augmented by transiently increasing extracellular signal-regulated kinase (ERK) activity through pharmacological inhibition of dual-specificity phosphatases 6 (DUSP6). The antidepressant-like behavioral effects of acute ketamine treatment were extended by DUSP6 inhibition for up to 2 months. The selective deletion of tropomyosin receptor kinase B (TrkB) in excitatory neurons abolished these DUSP6 inhibition-mediated synaptic and behavioral effects. These data suggest that ketamine's rapid antidepressant effects can be sustained by selectively targeting downstream intracellular signaling. - Source: PubMed
Publication date: 2025/05/08
Ma Z ZackGuzikowski Natalie JKim Ji-WoonKavalali Ege TMonteggia Lisa M