NTRK2 _ Trk_B _ TRKB Protein
- Known as:
- NTRK2 _ Trk_B _ TRKB Protein
- Catalog number:
- 10047-H03H
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- NTRK2 _ Trk_B TRKB Protein
Related genes to: NTRK2 _ Trk_B _ TRKB 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: NTRK2 _ Trk_B _ TRKB Protein
Related articles to: NTRK2 _ Trk_B _ TRKB Protein
- Adaptation is one of the key processes of animal domestication, environmental pressures will leave footprints in the genome. Geese are widely distributed across multiple geographical conditions with distinct adaptations. However, few reports have focused on the environmental adaptability of geese. Moreover, the key environmental drivers that trigger local adaptation and its genetic mechanisms are still unknown. To this end, 35 agro-climatic variables of 257 geese from 14 Chinese breeds were obtained, the key environmental drivers and its genetic mechanism were elucidated by combining the genome data. - Source: PubMed
Publication date: 2026/05/30
Zhou XiaoliXia JunliangChen WeidingZou JiajiaChen JiahuiZhang Xiquan - Accurate identification of gene fusions is critical for precision oncological approaches to sarcomas, where specific fusion genes are actionable targets of tyrosine kinase (TK) inhibitors. This study provides a descriptive overview of the real-world use, under a universal health insurance program, of 3 different comprehensive genomic profiling (CGP) panels within the Japanese national CGP system: GenMineTOP, which integrates DNA and RNA sequencing, and 2 DNA-based panels, FoundationOne CDx and the OncoGuide NCC Oncopanel System. - Source: PubMed
Publication date: 2026/05/27
Kamio SatoshiIkegami MasachikaKitada RinaMiwa SatoshiOgura KoichiIwata ShintaroKawai AkiraKobayashi EisukeSuehara YoshiyukiKohsaka Shinji - Tumours historically classified as extraventricular neurocytoma (EVN), initially in comparison with central neurocytoma, are defined by location and morphology; however, emerging molecular data demonstrate that this term is outdated. We report 14 previously unpublished tumours with a robust EVN DNA methylation profile, independent of original histopathologic diagnosis or anatomic location. Integrated molecular analyses identified FGFR1 alterations, particularly FGFR1::TACC1 fusions, as the predominant molecular driver of this tumour class. A smaller number of tumours harboured FGFR1 hotspot mutations (p.N546K and p.K656E). Among these, two cases additionally showed NF1 variants, and one tumour carried a PIK3CA mutation (p.H1047L). In addition, a single case exhibited an NTRK2 fusion. Histologically, tumours exhibited neurocytic differentiation with neuropil islands and a minor glial component, while immunohistochemistry showed frequent OLIG2 expression, contrasting with the typical immunophenotype of central neurocytoma. Notably, tumours with an EVN DNA methylation profile were identified in both extraventricular and intraventricular locations, demonstrating that anatomy-based definitions are inadequate for this tumour type. Clinical follow-up (median 33.2 months) showed predominantly lower grade behaviour, with occasional recurrence. Collectively, these findings support the view that tumours previously labelled as EVN do not represent a direct counterpart of central neurocytoma but instead constitute a molecularly and epigenetically distinct glioneuronal tumour type. We propose the designation glioneuronal tumour with neurocytic differentiation (GNTN) to reflect its biological identity and to align the terminology with contemporary molecular neuropathology, and recommend DNA methylation profiling as an essential diagnostic criterion. - Source: PubMed
Métais AliceEdjlali MyriamSassi FarahChotard GuillaumeUro-Coste EmmanuelleLhermitte BenoitAppay RomainPinto GiuseppeThomas ChristianBertero LucaRatliff MiriamKrieg Sandro Mvon Deimling AndreasSahm FelixVarlet PascaleSievers Philipp - Fusion involving , and are oncogenic driver occurring in several adult and pediatric tumor types. In sarcomas they are mostly found in infantile fibrosarcoma, inflammatory (IFS), inflammatory myofibroblastic tumor (IMT) and in the so-called "-rearranged spindle cell neoplasm" entity described in the current WHO (2020) classification, including lipofibromatosis-like neural tumor, fibrosarcoma-like and malignant peripheral nerve sheath tumor-like spindle cell neoplasms. - Source: PubMed
Cocchi StefaniaGambarotti MarcoGamberi GabriellaMagagnoli GiovannaMaioli MargheritaParra AlessandroSciulli EnricaIbrahim ToniRighi AlbertoBenini Stefania - Opioids are among the most widely prescribed treatments for pain; however, prolonged use leads to adverse effects, including tolerance and opioid-induced hyperalgesia. Neurons that detect noxious stimuli (nociceptors) within the dorsal root ganglion (DRG) are critical for both the analgesic and adverse effects of opioids. Although post-transcriptional RNA control is critical for DRG function, the role of circular RNAs (circRNAs), an evolutionarily conserved and highly stable class of RNA, in nociceptive processes remains largely unexplored. Furthermore, the effect of opioids on the circRNA landscape of human DRG (hDRG) is unknown. To address these gaps, we performed high-coverage total RNA sequencing on hDRG tissue obtained from opioid-exposed donors and compared circRNA and linear transcriptomic profiles to age- and sex-matched controls. Opioid exposure was associated with a global reduction in circRNA abundance, as well as specific alterations in 43 differentially expressed circRNAs. Parallel analysis of linear transcripts (mRNAs) revealed 349 differentially expressed transcripts, including genes involved in neuronal signaling and immune responses. Integrative circRNA-mRNA network analyses suggest that opioid-responsive circRNAs may modulate nociceptor gene expression through miRNA- and RNA-binding protein-binding mechanisms. Among opioid-associated circRNAs, circNTRK2, derived from NTRK2, the tyrosine kinase B receptor gene, was downregulated in both opioid-exposed hDRG tissue and a repeat morphine exposure paradigm in nociceptor-like cell line. Collectively, these findings establish the landscape of circRNAs in hDRG, reveal opioid-associated circRNA dysregulation, and highlight circRNAs as potential modulators of post-transcriptional gene expression in nociceptors. - Source: PubMed
Publication date: 2026/05/07
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