Ask about this productRelated genes to: CHN1 antibody
- Gene:
- CHN1 NIH gene
- Name:
- chimerin 1
- Previous symbol:
- CHN, DURS2
- Synonyms:
- RhoGAP2, ARHGAP2, n-chimerin
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-12
- Date modifiied:
- 2016-10-05
Related products to: CHN1 antibody
Related articles to: CHN1 antibody
- Across developmental stages, animals modulate their behavioural responses to external cues according to intrinsic physiological states. During development, particularly in juvenile stages, nervous systems undergo extensive changes at multiple levels. However, it remains unclear whether nervous systems at different developmental stages utilize the same underlying molecular mechanisms to produce equivalent behavioural modulations in response to intrinsic or extrinsic cues. Using the model organism Caenorhabditis elegans, we identify that animals employ distinct molecular mechanisms to achieve equivalent modulation of CO2-chemosensory behaviour at different developmental stages. Ubiquitin-proteasome-mediated downregulation of the insulin/IGF receptor, DAF-2, by the conserved quality-control ubiquitin ligase CHN-1/CHIP in the CO2-sensing BAG neurons promotes attraction to environmental CO2 during the starvation-induced L1-arrest stage. In contrast, CO2-attraction in dauer animals is independent of CHN-1/CHIP activity. Furthermore, the feeding-induced reversal of CO2-chemotaxis to avoidance during L1-arrest exit requires the insulin/IGF pathway and the conserved CRH-1/CREB1 transcription factor activity in the BAG neurons. However, the onset of CO2-avoidance during dauer exit is independent of CRH-1/CREB1 activity. These findings suggest that neural circuits at different life stages may utilize distinct, stage-specific molecular mechanisms to induce identical plasticity in chemosensory behaviour. - Source: PubMed
Publication date: 2026/09/24
Sahu Akankshya RamkrishnaMallick SwarupaVats AtalBhattacharya Abhishek - CXCL13 T cells and LAMP3 dendritic cells (DCs) are pivotal players in orchestrating anti-tumor immune responses, particularly within tumor tertiary lymphoid structures (TLS). However, their heterogeneity, differentiation trajectories, and clinical relevance in bladder cancer remain incompletely defined. This study integrated single-cell RNA sequencing (scRNA-seq) data (16 bladder cancer patients, 113,905 post-quality-control cells) and spatial transcriptomics to characterize CXCL13 T cell/LAMP3 DC subsets, their differentiation pathways (via Velocyto trajectory analysis), and intercellular crosstalk (via receptor-ligand mapping). A risk model (DTscore) was constructed using marker genes of these cells and validated in the IMvigor210 (atezolizumab-treated bladder cancer) and TCGA-BLCA cohorts. scRNA-seq clustering identified 10 immune and 3 nonimmune cell types, with T cells stratified into 8 subpopulations (including CD4CXCL13 T cells and CD8CXCL13 T cells) and DCs into 9 subgroups (including LAMP3 DCs). Receptor-ligand mapping and spatial transcriptomics confirmed functional crosstalk between CXCL13 T cells and LAMP3 DCs via key pairs (e.g., CCR7-CCL19, CXCR5-CXCL13, PDCD1-CD274) within TLS. The DTscore was developed using 8 marker genes (TSHZ2, ALOX5AP, GADD45G, TXN, CHN1, CCL19, CXCL13, ICA1) and exhibited robust prognostic and predictive performance: In the IMvigor210 cohort, high DTscore correlated with significantly poorer overall survival (OS) and a 3.27-fold lower immunotherapy response rate (11% vs. 36%, p = 4.23e-07); multivariate Cox regression confirmed DTscore as an independent OS predictor (hazard ratio = 1.97, p < 0.001). DTscore retained prognostic value in TCGA-BLCA (OS: p = 0.003; disease-specific survival: p < 0.001) and effectively predicted atezolizumab response even in the "immune desert" phenotype (p = 0.04). Combining DTscore with tumor mutational burden/tumor neoantigen burden yielded an AUC of 0.8122 for response prediction. Additionally, high DTscore was associated with higher OS hazard ratios in patients with wild-type TTN, RB1, EP300, or FGFR3 (all p < 0.01), while FGFR3 mutations correlated with lower immune checkpoint/CXCL13 expression. This study delineates the heterogeneity and interactions of CXCL13 T cell/LAMP3 DC subsets in bladder cancer TLS and validates DTscore as a robust tool for predicting OS and immunotherapy response, offering a potential guide for personalized bladder cancer treatment. - Source: PubMed
Publication date: 2026/08/05
Zhou LinZhu JinchaoLiu YushanXu Bin - Congenital cranial dysinnervation disorders (CCDDs) are a group of rare, nonprogressive conditions characterized by abnormal development of the cranial motor nerves and variable ocular motility deficits, ptosis, incomitant strabismus, and facial palsy. Advances in genetics and neuroimaging have revealed that these disorders result from defects in neuronal differentiation or axon guidance of the cranial motor neurons. Duane retraction syndrome, the most common CCDD, results from the absence of the abducens nerve and innervation of the lateral rectus by oculomotor nerve axons; causative genes include CHN1, MAFB, HOXA1, SALL4, and EBF3, although most cases do not have a genetic diagnosis. Congenital fibrosis of the extraocular muscles (CFEOM), results from variants in KIF21A, PHOX2A, TUBB3, or other tubulin genes, and affects the oculomotor and trochlear nerves. Horizontal gaze palsy with progressive scoliosis (HGPPS), caused by ROBO3 loss of function, arises from failure of axonal midline crossing in the brainstem. Moebius syndrome, defined by abducens and facial nerve palsies, has no identified genetic cause and may result from non-Mendelian causes. Additional CCDDs with atypical or syndromic presentations are linked to COL25A1, ECEL1, and ACKR3, although many do not have a genetic explanation. The expanding list of CCDD-associated genes highlights shared developmental pathways, including neuronal differentiation, axon guidance, and microtubule dynamics. Improved genetic diagnosis informs prognosis and multidisciplinary management. This review synthesizes current understanding of CCDDs, emphasizing the shift from phenotypic classification to molecular subtyping, and underscores the importance of ongoing research to resolve genetically unsolved cases and refine diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2026/03/23
Aufderheide KathleenWhitman Mary C - Spinal cord injury (SCI) is a highly disabling neurological condition that remains a worldwide challenge in healthcare. Our previous studies found that repetitive trans-spinal magnetic stimulation (rTSMS) applied at the L2 spinal segment yielded the most significant improvement in motor function in rats with SCI; however, the underlying mechanism remains unclear. Recent research indicates that disruption of the EphA4 signaling pathway in glutamatergic interneurons within the spinal cord leads to a loss of motor rhythm and a hopping gait in rats. Conversely, activating the locomotor central pattern generator (CPG) located in the L1-2 spinal segments promotes the recovery of motor function. Thus, by examining the effects of rTSMS on proteins associated with the EphA4 signaling pathway, this study provides novel insights for future investigations into its potential mechanisms of action. - Source: PubMed
Publication date: 2026/01/16
Liu HaoFang YuDeng QianYe JiucaiZhou JielanLuo Rong
- Source: PubMed