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
Ask about this productRelated 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
- 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
Koch Maddy RDemeter Jenna BHochrein MadisonAlles Sascha R AWestlund Karin NEhsanian Rezade la Peña June Bryan I - Neuroimaging studies suggest that Foreign Language Learning (FLL) influences resting-state functional connectivity (rs-FC) within the neocortex, but its effects on subcortical-cortical connectivity remain unclear. We hypothesize that FLL may specifically affect the rs-FC of subcortical regions involved in integrating cortical networks, leading to adaptive changes in overall brain connectivity. - Source: PubMed
Publication date: 2026/04/23
Bubbico GiovannaTomaiuolo FedericaSestieri CarloAkhlaghipour GolnoushGranzotto AlbertoFerretti AntonioPerrucci Mauro GianniSensi Stefano LDelli Pizzi Stefano - Radiation-induced gliomas (RIGs) can occur in regions of the central nervous system (CNS) previously irradiated for primary malignancies including leukemia, medulloblastoma, and ependymoma. Prognosis is uniformly poor despite treatment with standard of care therapy with radiation ± alkylating chemotherapy. Recent studies have shown that a subset of patients have gene fusions in targetable receptor tyrosine kinases (RTKs) including MET, NTRK2, and RAF1. However, clinical response and outcome to targeted therapy in this patient population have not been described. - Source: PubMed
Publication date: 2026/04/28
Ford NolanDlouhy Brian JGreenlee Jeremy DBuatti John MCleppe JasonMa DeqinEschbacher Kathryn LAbath Neto Osorio LopesGroves Andrew - Brain-derived neurotrophic factor (BDNF) and its high-affinity receptor tropomyosin receptor kinase B (TrkB) are classically associated with neuroplasticity, but increasing evidence suggests a broader role for BDNF/TrkB signaling in systemic stress adaptation beyond the central nervous system. Strenuous exercise is a model of functional stress that may become a clinically relevant renal challenge under conditions such as dehydration, heat stress, vascular vulnerability, and repeated exposure. Neuroendocrine stress activation, hemodynamic perturbations, and cytoskeletal instability are key factors that may contribute to glomerular barrier dysfunction in this setting. BDNF biogenesis is complex, and circulating BDNF largely reflects platelet-associated pools and context-dependent release. At the tissue level, BDNF/TrkB signaling can activate actin-regulatory pathways involved in cellular resilience. The podocyte is of particular interest because its actin-dependent architecture functionally parallels that of neurons and is essential for maintenance of the glomerular filtration barrier. Within this framework, BDNF/TrkB signaling may stabilize podocyte actin dynamics, reduce foot process effacement, and attenuate proteinuria. The present review focuses on the brain-kidney axis and the potential renoprotective role of BDNF/TrkB signaling, while highlighting major knowledge gaps regarding BDNF availability to glomerular cells, isoform-specific TrkB actions, and causal inference in humans exposed to repeated exercise-related renal stress. However, current human evidence is insufficient to define the dominant source and delivery route of BDNF to glomerular cells during exercise-related renal stress. Therefore, BDNF/TrkB is discussed here as a candidate modulatory/resilience pathway rather than an established causal driver. - Source: PubMed
Publication date: 2026/04/29
Beknazarova AnnaKuvaeva VictoriaBaltin MaximMutig KerimBobylev Alexander