CPLX1 Antibody
- Known as:
- CPLX1 Antibody
- Catalog number:
- XW-7950
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CPLX1 Antibody
Related genes to: CPLX1 Antibody
- Gene:
- CPLX1 NIH gene
- Name:
- complexin 1
- Previous symbol:
- -
- Synonyms:
- CPX-I
- Chromosome:
- 4p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-09
- Date modifiied:
- 2015-08-28
Related products to: CPLX1 Antibody
Related articles to: CPLX1 Antibody
- Spinocerebellar Ataxia type 2 (SCA2) and Amyotrophic Lateral Sclerosis type 13 (ALS13) are triggered by polyglutamine expansion in Ataxin-2 (ATXN2). To understand these neurodegenerative disorders at the molecular level, the brains of 10-month-old -CAG100-knockin mice were analyzed as microglial, astroglial and neuronal fractions via global RNA sequencing. Data were validated by comparison with the spinal cord oligonucleotide microarray profile or filtered by RNA-seq consistency. Here, we show that the mutation causes a massive inflammatory response in microglia and a reciprocal loss of neuronal transcripts in glial fractions, suggesting severe synapse loss. Beyond these general neurodegenerative signs, we identify pathognomonic changes in the machinery for protein translation and RNA splicing. Glial fractions showed upregulation of (to 2082%), , , , , , , , and as an unspecific neuroinflammatory signature, versus downregulation of axonal (to <19%), and synaptic , , , and mRNAs correlating with circuit disconnection. In all fractions, reductions in , , and were noted versus disease-specific inductions of ribosomal subunits, presumably mirroring the partial loss-of-function of ATXN2 as RNA translation modulator. Selective accumulations of embryonic factors and versus downregulation of adult specify the mutation impact on splicing and translation elongation. As a potential underpinning of toxic gain-of-function, the proteostasis transcript appeared increased in astroglial and microglial fractions. These transcriptome data suggest altered ribosomal and spliceosome machinery, with massive microgliosis versus mild astrogliosis, at the core of SCA2 and ALS13. - Source: PubMed
Publication date: 2026/04/15
Auburger GeorgKandi Arvind ReddyVutukuri RajkumarAlmaguer-Mederos Luis-EnriqueGispert SuzanaSen Nesli-EceKey Jana - Allele-specific expression (ASE) of long non-coding RNAs (lncRNAs) links genetic variation to synaptic dysfunction in psychiatric disorders. We previously identified a disease-associated ASE shift in LINC02449 at rs149707223 (C/G), with preferential expression of the alternative G allele in bipolar disorder (BD) and schizophrenia (SZ). Overexpression of LINC02449-G induced social deficits, repetitive behaviors, and enhanced excitatory synaptic transmission in the medial prefrontal cortex-nucleus accumbens (mPFC-NAc) circuit via upregulation of CPLX1. We hypothesized that these abnormalities are mediated by glutamatergic hyperexcitability and are pharmacologically reversible. - Source: PubMed
Ni ChaoyingLiu Jin-MingYang TengfeiDeng ZhiyingWu XiaohuiLi ShufenXue HannahWang ZhongjuCao XiongZhao Cunyou - Bipolar disorder (BD) and schizophrenia (SZ) are complex psychiatric disorders with overlapping features. Their heterogeneity may arise from interactions between genetic variants and environmental or epigenetic modifiers. Allele-specific expression (ASE), an imbalance in expression between gene alleles, provides a key mechanism linking these interactions to disease. We conducted transcriptomic and genomic analyses in phenotype-discordant monozygotic twins to investigate ASE in psychiatric risk. Nine ASE-affected long non-coding RNAs were identified, including LINC02449, which showed a consistent allele-specific shift in BD/SZ patients favoring the alternative G allele at rs149707223. Functional analyses revealed that overexpression of the LINC02449 G allele in mice induced social deficits and repetitive behaviors. These phenotypes were associated with enhanced excitatory transmission within the mPFC-NAc circuit, mediated by the synaptic regulator CPLX1. Our findings demonstrate that ASE-driven dysregulation of LINC02449 contributes to synaptic and behavioral abnormalities, underscoring ASE as a potentially important regulatory mechanism in BD and SZ pathogenesis. - Source: PubMed
Publication date: 2025/11/04
Yang TengfeiLiu Jin-MingChen QiaqiDeng ZhiyingNi ChaoyingWang YunqianLan YutingJiang TingyunLi ShufenJiang MeijunXue HongCao XiongWang ZhongjuZhao Cunyou - The amygdala participates in the processing of stimulus signals from stimuli and the coordination of the physiological and behavioral responses. The sexually dimorphic structure of the amygdala also contributes to sex-specific molecular and functional profiles. The present study compares the response of the amygdala molecular mechanisms to different environmental stimuli between sexes. The amygdala of female and male pigs was profiled under control, immunostimulation, and the metabolic stimulus of fasting using RNA-sequencing. Differential expression analysis (False Discovery Rate -adjusted p value < 0.05) identified 958 genes affected by stimulus and 504 genes affected by sex within treatments. The functional categories presenting a predominance of differentially expressed genes included the synaptic vesicle cycle pathway, vascular smooth muscle contraction pathway, epithelial cell proliferation process, chemokine signaling, and apoptosis. Network analysis revealed hub genes, including Stx1a, Cplx1, Clam3, and Myh11, among the gene modules susceptible to stimuli. The regulatory element SUZ12 was associated with differential gene expression between stimuli in both sexes, whereas RELA and IRF1 were uniquely detected in males and females, respectively. The findings from the multifaceted approach provide genomic leads to investigating interventions that can mitigate the effects of stimuli on the amygdala function. - Source: PubMed
Bhamidi SreelayaSunderland Gloria RSouthey Bruce RVillamil Maria BJohnson Rodney WRodriguez-Zas Sandra L - Menopausal syndrome (MPS) is a symptom of physical and psychosomatic abnormalities that women may face around the time of menopause. Hot flashes are the main symptom. Paeonia lactiflora extract (PLE) is the active ingredient extracted from . It can be used to treat MPS, such as hot flashes. However, its pharmacologic mechanism is unclear. - Source: PubMed
Publication date: 2025/07/22
Cui WeilinSong TingtingGao DongmeiWang XiaoyuSun YaFu LiyuHan YichaoWang Jieqiong