Ask about this productRelated genes to: NCKIPSD Blocking Peptide
- Gene:
- NCKIPSD NIH gene
- Name:
- NCK interacting protein with SH3 domain
- Previous symbol:
- -
- Synonyms:
- AF3P21, SPIN90, ORF1, WISH, WASLBP, DIP1
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-26
- Date modifiied:
- 2016-10-05
Related products to: NCKIPSD Blocking Peptide
Related articles to: NCKIPSD Blocking Peptide
- Eating disorder (ED) and obsessive-compulsive disorder (OCD) exhibit clinical and genetic overlap, yet whether they converge at the molecular level in the human brain is unknown. We perform large-scale transcriptomic profiling of the dorsolateral prefrontal cortex (DLPFC) and caudate in postmortem tissue from 86 controls, 57 individuals with ED, and 27 with OCD. ED shows robust, region-specific transcriptional dysregulation (102 differentially expressed genes [DEGs] in DLPFC and 222 in caudate at FDR <1%) that replicates in an independent cohort. OCD shows no single-cohort DEGs, but meta-analysis across three datasets identifies 57 caudate-associated genes. Despite these differences, transcriptome-wide effects strongly correlate between ED and OCD (DLPFC r = 0.67; caudate r = 0.75), indicating shared molecular pathology. Joint ED + OCD analysis identifies 233 DEGs in DLPFC and 815 in caudate, implicating GABAergic signaling, neuroendocrine regulation, mitochondrial metabolism, and CHD8-associated networks. Genetically regulated expression analyses identifies five genes (WDR6, NCKIPSD, P4HTM, DALRD3, and SHISA5) with convergent risk associations across disorders and brain regions, all mapping to a gene-dense region on chromosome 3. These findings define a shared cortico-striatal transcriptional architecture and identify candidate genes for transdiagnostic intervention. - Source: PubMed
Publication date: 2026/06/15
Breen Michael STao RanYang AndyWang XuranAmini PardisRodriguez de Los Santos MiguelBrandtjen Anna CDeep-Soboslay AmyKaye Walter HHyde Thomas MKleinman Joel EBuxbaum Joseph DGrice Dorothy E - Arp2/3 complex is a key nucleator of actin filaments. It requires activation by nucleation-promoting factors (NPFs). WISH/DIP1/SPIN90 (WDS) proteins represent a unique class of NPFs that activate the Arp2/3 complex independently of preexisting filaments, promoting linear actin-filament nucleation. In fission yeast, Dip1 binds to the clamp subunits in Arp2/3 complex to induce the short-pitch conformation, where Arp2 moves closer to Arp3 to mimic a filamentous actin dimer. However, how WDS proteins stimulate subunit flattening in Arp subunits, a 'scissor-like' conformational change akin to what is observed in an actin monomer during filament formation, remained unclear. Here we present cryo-electron microscopy structures of human SPIN90 bound to activated bovine Arp2/3 complex on an actin filament pointed end. The structures show that SPIN90 dimerizes through a metazoan-specific domain in the middle segment, engaging both the clamp and the Arp3/ARPC3 interface, to drive the activating conformational changes in Arp2/3 complex. Remarkably, a single SPIN90 dimer can also bridge two Arp2/3 complexes, enabling bidirectional actin nucleation and suggesting a mechanism for rapidly assembling complex actin network architectures. - Source: PubMed
Publication date: 2025/09/15
Francis JustusPathri Achyutha KrishnaShyam Kankipati TejaSripada SridharMitra RishavNarvaez-Ortiz Heidy YEliyan Kiran VyshnavNolen Brad JChowdhury Saikat - An epidemiological association between anxiety and stroke is well-established; however, the role of shared genetic factors remain unclear. This study aimed to investigate the shared genetic architecture between anxiety and stroke. - Source: PubMed
Publication date: 2024/12/15
Zhang YichenJiang Yong'AnFan HengyiYuan RaoraoCai JianhuiZhong BoQin QianZhang ZileZhang YanCheng Shiqi - Ras-related associated with diabetes (RRAD) is a member of the Ras GTPase superfamily that plays a role in several cellular functions, such as cell proliferation and differentiation. In particular, the superfamily acts as an NF-κB signaling pathway inhibitor and calcium regulator to participate in the immune response pathway. A recent transcriptome study revealed that was expressed in the spleen of disease-resistant Japanese flounder () individuals compared with disease-susceptible individuals, and the results were also verified by qPCR. Thus, the present study aimed to explore how regulates antimicrobial immunity via the NF-κB pathway. First, the coding sequence of was identified. The sequence was 1092 bp in length, encoding 364 amino acids. Based on and structural relationship analyses, appeared to be more closely related to teleosts. Next, expression differences between disease-resistant and disease-susceptible individuals in immune-related tissues were evaluated, and the results revealed that was expressed preferentially in the spleen of disease-resistant individuals. In response to infection, expression in the spleen changed. In vitro, co-culture was carried out to assess the hypo-methylated levels of the promoter in the disease-resistant spleen, which was consistent with the high mRNA expression. The siRNA-mediated knockdown of performed with the gill cell line of affected many -network-related genes, i.e., , , , , , , , , , , , and others, as well as some inflammation-related genes, such as and . In addition, flow cytometry analysis showed that overexpression was more likely to induce cell apoptosis, with establishing a link between 's function and its potential roles in regulating the NF-κB pathway. Thus,. the current study provided some clarity in terms of understanding the immune response about rrad gene differences between disease-resistant and disease-susceptible individuals. This study provides a molecular basis for fish gene functional analysis and may serve as a reference for in-depth of bacterial disease resistance of teleost. - Source: PubMed
Publication date: 2024/10/01
Zhu YingYang XinshengYang YingmingYan XuLi ChaoChen Songlin - Anorexia nervosa (AN) is a devastating disorder with evidence of underexplored heritability. Twin and family studies estimate heritability (h ) to be 57%-64%, and genome-wide association studies (GWAS) reveal significant genetic correlations with psychiatric and anthropometric traits and a total of nine genome-wide significant loci. Whether significantly associated single nucleotide polymorphisms identified by GWAS are causal or tag true causal variants, remains to be elucidated. We propose a novel method for bridging this knowledge gap by fine-mapping short structural variants (SSVs) in and around GWAS-identified loci. SSV fine-mapping of loci associated with complex disorders such as schizophrenia, amyotrophic lateral sclerosis, and Alzheimer's disease has uncovered genetic risk markers, phenotypic variability between patients, new pathological mechanisms, and potential therapeutic targets. We analyze previous investigations' methods and propose utilizing an evaluation algorithm to prioritize 10 SSVs for each of the top two AN GWAS-identified loci followed by Sanger sequencing and fragment analysis via capillary electrophoresis to characterize these SSVs for case/control association studies. Success of previous SSV analyses in complex disorders and effective utilization of similar methodologies supports our proposed method. Furthermore, the structural and spatial properties of the 10 SSVs identified for each of the top two AN GWAS-associated loci, cell adhesion molecule 1 (CADM1) and NCK interacting protein with SH3 domain (NCKIPSD), are similar to previous studies. We propose SSV fine-mapping of AN-associated loci will identify causal genetic architecture. Deepening understandings of AN may lead to novel therapeutic targets and subsequently increase quality-of-life for individuals living with the illness. PUBLIC SIGNIFICANCE STATEMENT: Anorexia nervosa is a severe and complex illness, arising from a combination of environmental and genetic factors. Recent studies estimate the contribution of genetic variability; however, the specific DNA sequences and how they contribute remain unknown. We present a novel approach, arguing that the genetic variant class, short structural variants, could answer this knowledge gap and allow development of biologically targeted therapeutics, improving quality-of-life and patient outcomes for affected individuals. - Source: PubMed
Publication date: 2022/04/26
Berthold NatashaPytte JuliaBulik Cynthia MTschochner MonikaMedland Sarah EAkkari Patrick Anthony