Ask about this productRelated genes to: CRMP1 Blocking Peptide
- Gene:
- CRMP1 NIH gene
- Name:
- collapsin response mediator protein 1
- Previous symbol:
- -
- Synonyms:
- DRP-1, DPYSL1
- Chromosome:
- 4p16.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-01-16
- Date modifiied:
- 2016-10-05
Related products to: CRMP1 Blocking Peptide
Related articles to: CRMP1 Blocking Peptide
- Keel length is a key body size indicator, which has an important impact on the overall growth performance, bone health, and production performance of poultry. In the process of selecting crossed strains for yellow feathered broiler chickens, it is generally necessary to select keel length, but there is little research on keel length development. Therefore, resequencing and GWAS was employed to obtain SNP molecular markers associated with keel length in a specialized Yellow-feathered broiler line. We identified 10 SNPs that were potentially significantly correlated with keel length for the first time located at 9 genes, including ATP7B, CST3, OTOP1, CRMP1, SLC12A1, COPS2, FAM227B, IFT140, APLP2. SNP2 and SNP3 loci were in a strongly linked state (D ' value=1), the other 8 SNP loci were not in a strongly linked state (D 'value<1). The association analysis between single SNP marker and keel length traits showed that TT and CT at SNP1 (rs315701680), GG at SNP2 (rs738740137), AA at SNP3 (rs317223723), AA at SNP4 (rs732443622), GG at SNP5(rs315667756), CC at SNP6 (rs314381113), GG at SNP7 (rs732811384), TT at SNP8 (rs314197610), CC and TC at SNP9 (rs13782000), TT and GT at SNP10 (rs737401141) genotypes were all the dominant genotypes for keel length. The strong linkage between SNP2 and SNP3 resulted in two haplotypes H1 (AG) and H2 (GA), respectively. The H1H1 haplotype (GGAA) produced by SNP2 and SNP3 linkage was the dominant genotype for keel length. The SNP molecular markers and dominant genotypes at SNP1-SNP10 loci identified in this study may be used to improve the accuracy and genetic progress of keel length selection. Meanwhile, candidate genes potentially significantly related to keel length will lay the foundation for genetic selection of keel length and cultivation of high-quality yellow feathered broilers in the future. - Source: PubMed
Publication date: 2026/03/27
Tu Y JLiu Y FZhang MJu X JShan Y JJi G GShu J T - Patients with high-risk neuroblastoma (NB) continue to have long-term survival rates below 60%, with relapse occurring in more than half of patients, likely driven by chemoresistant minimal residual disease in the bone marrow (BM-MRD). Although several quantitative PCR (qPCR) and droplet digital PCR (ddPCR) assays measuring different but overlapping sets of NB-associated mRNAs (NB-mRNAs) have shown a significant prognostic value at various time points, the optimal combination of MRD markers (a set of NB-mRNAs) and evaluation timing remains unclear. In the present study, 89 bone marrow samples were collected from mostly overlapping 30 high-risk NB patients at four time points: diagnosis (Dx), end of induction (EOI), end of high-dose chemotherapy (EOH), and end of consolidation (EOC). BM-MRD was assessed with a 7NB-mRNAs ddPCR assay quantifying CRMP1, DBH, DDC, GAP43, ISL1, PHOX2B, and TH mRNAs. BM-MRD at EOH and EOC time points was significantly associated with relapse. Moreover, patients with higher BM-MRD levels at EOH (7NB-mRNAs ≥ 3.5) and EOC (7NB-mRNAs ≥ 3.5) time points had significantly inferior 3-year event-free survival (EOH, = 0.003; EOC, = 0.033). These results indicate that EOH and EOC are clinically informative evaluation time points for BM-MRD detected by 7NB-mRNA expression. - Source: PubMed
Publication date: 2026/03/05
Mon Cho YeeNay Win Kaung HtetNishimura AkihiroNakatani NaokoTamura AkihiroYamamoto NobuyukiNino NanakoUemura SuguruSaito AtsuroIshida ToshiakiMori TakeshiHasegawa DaiichiroOkuno KeisukeKosaka YoshiyukiIshizawa KikyoUmemoto MayunoMatsui TaiseiNagatani AyakaNishimura Noriyuki - An emerging area of research into major mental illnesses is to investigate the formation of insoluble aggregates of specific proteins in the brains of patients with these conditions. These studies are normally based on examining insoluble protein in post mortem brain samples, but, for practical reasons, typically consider only one region of the brain per subject. Here, we tested post mortem brain samples from multiple brain regions of various individuals, which included patients with major depressive disorder, schizophrenia and victims of suicide. Samples from patients with Alzheimer's disease and control individuals were used for comparison. Notably, 20 tissue samples were available from across the brain of one individual who had both schizophrenia and Alzheimer's disease. Consistently, while insolubility of DISC1 (Disrupted in Schizophrenia 1), CRMP1 (Collapsin Response Mediator Protein 1) and/or TRIOBP-1 (Trio and F-actin Binding Protein, isoform 1) were often present in multiple brain regions, this was not homogenous across the brain. While this study looks at a relatively small number of subjects, and caution must be taken in over-generalising, it is possible that aggregation of these proteins spreads throughout the brain, in a similar manner to the staging seen in neurodegenerative disease. Previous studies may therefore have underestimated the prevalence of protein aggregation in mental illness, due to this heterogeneity of insoluble protein across the brain. - Source: PubMed
Publication date: 2026/02/11
Samardžija BobanaRenner ÉvaPalkovits MiklósBradshaw Nicholas J - : Suicide is a significant public health concern with a multifactorial etiology. The biological background of suicide is not sufficiently explored, which encumbers suicide prevention. Epigenetic mechanisms may mediate environmental influences on suicide risk. Recent studies have suggested that protein aggregation occurs in the brains of patients with chronic psychiatric disorders and suicidality, which may influence disease trajectory. However, the intersection between epigenetics and proteinopathy in suicide remains unexplored. Our pilot study investigated whether aggregation-related genes show epigenetic and transcriptional alterations in the post-mortem brains of individuals who had died by suicide. : Brain tissue from 69 male subjects (32 suicide by hanging, 37 sudden cardiac death controls) was collected at autopsy. Genome-wide hippocampal DNA methylation data from our previous reduced representation bisulfite sequencing (RRBS) study were reanalyzed to identify differentially methylated cytosines (DMCs) in candidate aggregation-related genes. The expression of nine candidate and three reference genes in the hippocampus and Brodmann area 46 was assessed by qPCR. Statistical analyses were performed using Student's -test or Mann-Whitney U test ( < 0.05 was considered significant). Reanalysis revealed hypomethylation in suicide cases within , , , , , , and . In the hippocampus, suicides exhibited increased expression of , , , , and , and decreased expression. The ratio was significantly elevated. In Brodmann area 46, altered expression was limited to increased and decreased . : This is the first study to implicate epigenetic and transcriptional dysregulation of protein aggregation-associated genes in suicide. The findings suggest a possible role for proteostasis disturbances in suicidality, particularly within the hippocampal pathways related to stress response and synaptic signaling. Validation in larger cohorts and protein-level studies are warranted to determine the functional significance of these findings. - Source: PubMed
Publication date: 2025/12/08
Bedene TajaŠmon JulijaVidetič Paska AljaZupanc TomažKouter Katarina - Schizophrenia is a severe psychiatric disorder marked by significant cognitive, perceptual, and social deficits, the neurobiological basis of which remains incompletely elucidated. Increasing evidence implicates disruptions in protein homeostasis, including misfolding and aggregation of key neuronal proteins, as contributing factors to its pathogenesis. While proteinopathies have been extensively studied in neurodegenerative diseases, their role in schizophrenia has only recently gained attention. Central to these processes is endoplasmic reticulum (ER) stress and the activation of the unfolded protein response, which regulate protein folding and cellular quality control. Dysregulation of ER stress pathways, alongside impaired chaperone protein function and mitochondrial dysfunction, can lead to accumulation of misfolded proteins and neuronal dysfunction. Proteins such as DISC1, CRMP1, NOS1AP, and others have been identified with altered expression and aggregation patterns in schizophrenia, linking protein abnormalities to disease pathology. Additionally, mounting evidence suggests that chronic ER stress can activate microglia, the brain's immune cells, triggering the release of proinflammatory cytokines and promoting neuroinflammation. Sigma-1 receptor, a unique ER chaperone protein involved in modulating ER stress and calcium signaling, has emerged as a critical regulator of neuronal proteostasis and survival. Agonists of the sigma-1 receptor show promising therapeutic potential by alleviating ER stress, enhancing neuroprotection, halting inflammation, and restoring cellular homeostasis in preclinical models of schizophrenia and other brain disorders. In this review, we will discuss these interconnected molecular mechanisms, highlighting novel therapeutic pathways focused on proteostasis restoration and sigma-1 receptor modulation, which offer a promising avenue for future interventions in schizophrenia. - Source: PubMed
Publication date: 2025/11/11
Ahmed Mariam KAbdou KareemIbrahim Weam WMohamed Ahmed FEl-Boghdady Noha A