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
- Genetic and environmental factors during early development contribute to autism pathogenesis. Maternal autoantibodies recognizing specific fetal brain proteins can predict autism risk in a subset of cases. These antibodies cross the placenta and bind to their target antigens, which play critical roles in neurodevelopment, thereby increasing autism risk in this mechanistically defined subtype, Maternal Autoantibody-Related Autism (MARA). A multi-ELISA assay that detects maternal autoantibody combinations associated with increased autism risk has been described in the literature. This study aimed to transfer the MARA related autoantibody component assays to a clinical development laboratory for optimization and performance characterization. Indirect ELISA assays for eight maternal autoantibodies targeting LDH-A, LDH-B, GAH, STI1, CRMP-1, CRMP-2, NSE, and YB-1 were transferred from an academic laboratory to a clinical development laboratory for optimization and determination of the analytical performance and preliminary assay cutoff values. Standard methodologies were used to assess linearity, sensitivity, specificity, precision, and stability. Predefined validation protocols based on professional guidelines with established acceptance criteria for each parameter were followed. Optimized ELISAs met the acceptable analytical performance criteria. All assays except one demonstrated excellent linearity when diluted with buffer or non-reactive plasma. The sensitivity analysis showed the lower limit of quantification discretely above the limit of detection, and below the preliminary population-based threshold values. Coefficients of variation for within-lot reproducibility of positive samples were <15%, with two minor exceptions. Common interfering substances, except whole human IgG, did not affect assay performance. Microtiter assay plates were stable for at least six months without significant assay drift. These maternal autoantibody assays demonstrated high sensitivity, specificity, and robustness, supporting progression to validation in CLIA-certified clinical laboratories. These assays will enable rigorous clinical evaluation of the accuracy of specific antibody combinations previously reported in the peer reviewed literature to specifically correlate with autism. - Source: PubMed
Publication date: 2026/05/28
McInerney MagsHurley BethBarkow JessicaMenning KatherineNicolace JustinSchauer JosephVan de Water JudyWassman E Robert - Maternal autoantibodies targeting neural proteins represent a major environmental contributor to autism spectrum disorder (ASD). Although anti-collapsin response mediator protein 1 (CRMP1) antibodies (Abs) have been detected in mothers of ASD children, the pathogenic role of anti-CRMP1 Ab in ASD remains unclear. Here, we evaluated the ability of maternal anti-CRMP1 Ab to induce pathology in a mouse model. Using a cell-based assay, we found that maternal anti-CRMP1 Ab persisted throughout gestation and was detected in offspring serum on postnatal day 16. Exposed offspring exhibited delayed developmental milestones during the neonatal period. During adolescence, exposed mice buried more marbles, spent more time self-grooming and enhanced central zone exploration in the open field test without changes in elevated plus maze, suggesting increased repetitive stereotyped behaviors and sensory hyposensitivity. Transcriptomic analysis of the offspring cortex on postnatal day 30 revealed upregulation of positive regulation of cholinergic synaptic transmission and downregulation of pathways related to axon guidance and presynaptic membrane organization. We further confirmed that the expression of genes associated with presynaptic membrane organization (Nrxn1, Pten, Ptprd, Nlgn1) were significantly reduced, suggesting that anti-CRMP1 Ab interferes with axon development. In vitro, anti-CRMP1 Ab treatment induced more growth cone collapse in iPSC-derived immature neurons without affecting basic neurite morphology. Collectively, we demonstrate that maternal anti-CRMP1 Ab leads to ASD-like behaviors in offspring and induces more growth cone to disrupt early neurodevelopment, thereby establishing single maternal anti-CRMP1 Ab as an important pathogenic factor for ASD. - Source: PubMed
Publication date: 2026/06/01
Pan YueYuan ZhirongChen ZiruiSun WeiWu PengchengWu XiaojunHu XinyueLai ZhaohuiHu Yafang - Suicide is a major public health concern and cause of death worldwide. While progress has been made in understanding molecular pathways involved in suicide, much more work is needed to identify clinically useful biomarkers of suicidality. Disturbed cellular proteostasis and aggregation of specific misfolded proteins are established pathological factors of neurodegenerative diseases. Increasing evidence also suggests that such aggregates often occur in patients with chronic mental illnesses. Recently, genes related to disturbed proteostasis showed differential methylation in individuals who died by suicide compared to controls. These include five genes encoding proteins that aggregate in neurodegenerative and/or mental illness: (also called ), , (encoding the Tau protein), (also called , encoding Parkin), and . Given the possibility that altered methylation in these genes could affect expression of the proteins they encode, we aimed to review evidence for whether disturbed proteostasis may be a point of overlap between suicidality, neurodegenerative disease, and/or mental illnesses. Epigenetic changes in most of these genes also occur in other neurological disorders. Autophagy, and, to a lesser extent, the ubiquitin-proteasome system, are emerging as potentially impaired in individuals with suicidal tendencies and individuals who died by suicide. Based on this accumulated data, we hypothesise that disturbed proteostasis is likely to be a pathological component of suicidality. It is also plausible that this may lead to the accumulation of aggregated proteins in a similar manner to, and potentially overlapping with, those seen in major mental illnesses. If true, this would have consequences for potential identification of biomarkers for suicidality and should be a priority for future research in the field. - Source: PubMed
Publication date: 2026/05/16
Šmon JulijaJuković MajaKršanac MateaSamardžija BobanaVidetič Paska AljaŽerovnik EvaKouter KatarinaBradshaw Nicholas J - 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