PPP3CA Antibody
- Known as:
- PPP3CA Antibody
- Catalog number:
- 32139
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- PPP3CA Antibody
Related genes to: PPP3CA Antibody
- Gene:
- PPP3CA NIH gene
- Name:
- protein phosphatase 3 catalytic subunit alpha
- Previous symbol:
- CALN, CALNA
- Synonyms:
- CNA1, PPP2B
- Chromosome:
- 4q24
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-26
- Date modifiied:
- 2016-02-10
Related products to: PPP3CA Antibody
Related articles to: PPP3CA Antibody
- In this study, we present the largest rare coding variant association study of schizophrenia to date, with 87,959 schizophrenia cases and 150,587 controls. We identify 16 genes at exome-wide significance: and and an additional 24 at a 5% false discovery rate. Cases carrying ultra-rare, damaging variants, primarily protein-truncating and deleterious missense mutations, show strong enrichment in constrained genes with consistent effects across ancestries. Half of the 40 identified genes overlap with those implicated in developmental delay, autism, or bipolar disorder, underscoring shared neurodevelopmental risk. All 40 genes identified are highly expressed in excitatory and inhibitory neurons, and their expression patterns span diverse developmental stages. Functionally, the identified genes implicate chromatin regulation, protein degradation, and synaptic function. Overall, our results advance understanding of the genetic architecture of schizophrenia, provide a foundation for modeling risk genes in cellular and animal systems, and offer a framework for future work toward biologically informed patient stratification. - Source: PubMed
Publication date: 2026/09/21
Sealock Julia MDowd ConnorLiao CalwingYe RobertHowrigan DanielSatterstrom F KyleAuwerx ChiaraKim SoyeonHuai CongHe LinAlemayehu MelkamGichuru StellaMwende Rehema MNewton Charles R J CKoen NastassjaZingela ZukiswaKyebuzibwa JosephStevenson AnneHassan ArsalanWang KaiArai MakotoHoriuchi YasueItokawa MasanariSerrano Nora AyolaBearden Carrie EBelangero Sintia ICastor Albuquerque Saulo GCrossley Nicolasde Souza Rodrigues Andre LDiaz-Zuluaga Ana MDiniz Mateus MFreitas Thiago HGadelha AryGomez-Makhinson JulianaHolanda NayanaKopelowicz AlexLorencetti Pedro GQuarantini Lucas CRamirez-Diaz Ana MReus Victor ISantoro Marcos LTeshiba TerriZiebold CarolinaSotelo-Ramirez Carlo EstebanSanabrais-Jiménez Marco AntonioHahn EricNguyen Van PhiLind Penelope AForsyth JenniferOkewole AdeniranGo Rodney C PGur RaquelGur RubenCraddock NicholasPalotie AarnoHämäläinen EijaPietiläinen OlliGlatt Stephen JHultman ChristinaLópez Celso ArangoMcQuillin AndrewBass NickPulver Ann ESt Clair DavidCohen BruceBlackwood Douglas HMcIntosh AndrewEsko TõnuKarlson ElizabethCorvin Aiden PMorris Derek WManoach DaraLanden Mikael Boehnke MichaelBørglum Anders DChurchhouse ClaireCurtis DavidO'Donovan Michael COwen Michael JRees ElliottSullivan Patrick FVawter Marquis PWalters James T RScott LauraMedland Sarah ENguyen Van TuanTa Thi Minh TamCamarena BeatrizFreimer NelsonLopez-Jaramillo CarlosOlde Loohuis LoesOphoff Roel ASawa AkiraPato Carlos NPato Michele TAyub MuhammadKnowles James AStroud RockyAtwoli LukoyeDickens AkenaKariuki Symon MKoenen Karestan CStein Dan JTeferra SolomonQin ShengyingDaly Mark JHuang HailiangNeale Benjamin M - In Alzheimer's disease (AD), amyloid beta (Aβ) plaques and hyperphosphorylated tau tangles drive neurodegeneration and cognitive decline. Disrupted calcium homeostasis-particularly via transient receptor potential canonical-1 (TRPC1) channels-contributes to tauopathy and disease progression. This study investigated the therapeutic potential of 2-aminoethoxydiphenyl borate (2-APB), a modulator of TRP channels, in a scopolamine-induced rat model of AD. Adult Wistar rats were assigned to six groups: normal control, disease control (scopolamine 2.5 mg/kg), three 2-APB treatment groups (2.5, 5.0 and 10.0 mg/kg) and a donepezil group (5.0 mg/kg), each with six animals. Treatments lasted three weeks. Cognitive performance was assessed using the Morris water maze, memory consolidation and open field tests. Biochemical assays measured acetylcholinesterase (AChE), calcineurin, oxidative stress markers (GSH, MDA) and inflammatory cytokines (TNF-α, IL-6, IL-1β). Protein and gene expression analyses (Western blot, qRT-PCR) evaluated tau, GSK-3β, TRPC1, MARK2, and calcineurin A/PPP3CA, alongside histopathological and immunohistochemical studies. 2-APB treatment significantly reduced pro-inflammatory cytokines, alleviated neuroinflammation, and decreased oxidative stress. Cognitive function improved, correlating with normalized AChE activity and preserved neuronal structure. At the molecular level, 2-APB reduced tau hyperphosphorylation at Ser396 and Thr231, likely through suppression of TRPC1-associated calcium entry and consequent modulation of calcium-dependent kinases (MARK2) and phosphatases (calcineurin), as well as the GSK-3β pathway. However, given that 2-APB is a broad-spectrum calcium signaling modulator - known to act on IP₃ receptors, SOCE/ORAI pathways, and multiple TRPC subtypes in addition to TRPC1-the present findings provide supportive evidence linking TRPC1 modulation to the observed neuroprotective effects. Although, the involvement of additional interconnected signaling mechanisms cannot be excluded and these findings should be interpreted within the context of 2-APB's pleiotropic pharmacological profile. Downregulation of TRPC1 and calcineurin A/PPP3CA gene expression supported 2-APB's role in restoring calcium balance and mitigating tau pathology. These results highlight 2-APB's potential in addressing key AD features-tauopathy, oxidative stress, neuroinflammation and cognitive impairment-warranting further preclinical and clinical research as a potential therapeutic for AD and related tauopathies. - Source: PubMed
Publication date: 2026/08/01
Kewal AkashRajput Mithun SinghShah JignaGandhi Dipal - Semen quality traits in chickens are critical indicators reflecting reproductive efficiency, breeding progress, and economic profitability in the poultry industry. Understanding the genetic architecture and enabling targeted genetic improvement of these traits are essential for enhancing poultry production efficiency. In this study, we estimated genetic parameters and performed weighted single-step GWAS for five semen traits in RIR chickens to reveal their genetic architecture and identify key candidate genes and QTLs associated with semen quality. The results showed that heritability estimates for SEVOL, SECON, SPMOT, SPABR, and SPCOUNT ranged from 0.097 to 0.322, indicating low to moderate heritability. 29 significant QTL regions and 12 candidate genes (NFKB1, UBE2D3, PPP3CA, EIF4E, H2AFZ, DOCK2, MTNR1A, TACC3, ADCYAP1, GFRA1, ABLIM1, and CASP7) associated with semen traits were identified by WssGWAS. These QTL regions were located on chromosomes 4 and 13 for SEVOL, chromosome 4 for SPMOT, and chromosomes 2 and 6 for SPABR. Interestingly, four prominent consecutive QTL regions were shared between SEVOL and SPMOT. These QTL were located at 59.83-61.43 Mb, explaining 11.55% and 16.33% of the genetic variance for SEVOL and SPMOT, respectively. The largest-effect SNPs within these four QTL intervals exhibited significant effects on both semen volume and sperm motility, and these markers could be used for marker-assisted selection of semen traits. This study provides further insights into the genetic architecture of chicken semen traits, improves our understanding of their molecular regulation, and identifies valuable QTL and candidate genes. These findings offer a scientific basis for genetic improvement and marker-assisted selection of semen quality. - Source: PubMed
Publication date: 2026/05/28
Tesfay Hailai HagosZhang XiaokeLi YunleiZong YunheMa ZhongHan XintongZhao YiPan ZitingMani Adamu IsaYang FujianZhang ZongyaoChen JimingSun YanyanChen Jilan - Benzo[a]pyrene (BaP), an air pollution-related polycyclic aromatic hydrocarbon, may intersect with molecular pathways relevant to atrial fibrillation (AF), but this relationship remains unclear. - Source: PubMed
Publication date: 2026/06/26
Wang QianchenWu JiejieQi ShaoyuZhang JingwenLiu Yang - Plasma proteomics and metabolomics snapshots reveal a molecular signature in circulation delineating pathophysiology of major and minor neurocognitive disorder. To identify new cues to disease aetiology and diagnostic approach, we applied plasma proteomics and metabolomics profiling platforms to samples collected in a population-based study of the Singapore Longitudinal Ageing Studies Wave 2 (SLAS-2). In this longitudinal study, blood samples were analysed with standard clinical chemistry, plasma proteomics (Sengenics) and metabolomics (Nightingale) panels. Participants were followed up for the development of mild cognitive impairment (MCI) and dementia for 3-5 years. Of the total 1,892 molecules in all assay types, 463 demonstrated significant associations with baseline prevalent MCI and dementia. We trained an automatic linear modelling of predictors for follow-up new-onset MCI and dementia. The best model consists of 10 variables including ZSCAN18, PRKD3, SPANXN4, DDX43, saturated fatty acids, PPP3CA, NFATC4, IL-8, PAK6, and PDGFB. In terms of molecular function, these molecular markers are involved in immunological dysfunction and inflammatory reaction, protein coding, lipids, DNA-binding transcription factor activity, and nervous system development. In conclusion, our current research has identified an omics signature linked to new-onset mild cognitive disorder and dementia, which we hope can help enhance the accuracy of their diagnosis using circulating blood samples. - Source: PubMed
Publication date: 2026/06/16
Lu YanxiaTan Crystal Tze YingGwee XinyiLarbi AnisNg Tze Pin