Ask about this productRelated genes to: PPP3R1 antibody
- Gene:
- PPP3R1 NIH gene
- Name:
- protein phosphatase 3 regulatory subunit B, alpha
- Previous symbol:
- -
- Synonyms:
- CALNB1, CNB, CNB1
- Chromosome:
- 2p14
- Locus Type:
- gene with protein product
- Date approved:
- 1993-01-25
- Date modifiied:
- 2015-11-18
Related products to: PPP3R1 antibody
Related articles to: PPP3R1 antibody
- Phenotypic plasticity allows organisms to adapt traits in response to environmental changes, yet the molecular basis by which such plastic traits become genetically fixed remains unclear. Here, we investigated gut-length plasticity in medaka fish () through genome-wide methylation profiling, CRISPR/Cas9-mediated deletion, and population genomic analyses. We found that seasonal methylation of CpG sites upstream of the is correlated with gut-length plasticity, and deletion of this region abolishes plasticity. Additionally, standing variation in is associated with genetically fixed longer gut length in populations lacking plasticity. These results suggest that loss of epigenetic regulation via CpG site reduction triggers the genetic fixation of novel traits. Our findings provide molecular evidence linking epigenetic plasticity and genetic assimilation, advancing understanding of plasticity-led evolution in natural populations. - Source: PubMed
Publication date: 2026/03/25
Katsumura TakafumiSato SuguruYamashita KanaOda ShojiGakuhari TakashiTanaka ShodaiFujitani KazukoNishimaki ToshiyukiImai TadashiYoshiura YasutoshiTakeshima HirohikoHashiguchi YasuyukiSekita YoichiMitani HiroshiOgawa MotoyukiTakeuchi HideakiOota Hiroki - Chronic venous disease (CVD) arises from venous hypertension secondary to impaired venous return, causing significant morbidity and diminished quality of life. Genetic factors are likely important in the pathogenesis and susceptibility of a patient to develop CVD. This systematic review summarizes genome-wide association studies (GWASs) that investigate the link between genetic variants and CVD. - Source: PubMed
Publication date: 2025/12/13
Soh Chien LinTan MatthewDavies Alun HOnida Sarah - Abnormal neurotransmitter regulation plays a role in the pathogenesis of Schizophrenia (SCZ), and the presence of brain tissue-like aberrant expression in the partial transcriptome of peripheral blood leukocytes from patients with SCZ suggests that these aberrantly expressed genes could be potential diagnostic markers. We designed a case-control study to analyze the association between the expression levels of mRNAs and SCZ in peripheral blood leukocytes and to explore their potential value as diagnostic biomarkers for SCZ. Differentially expressed mRNAs associated with neural signaling pathways were screened by RNA sequencing in a small set, comprising 9 patients with SCZ and 20 controls. A case-control study that included 217 cases and 217 controls was further conducted to verify these mRNAs. The differential expression analysis between cases and controls was performed, followed by restricted cubic spline regression analysis. Gene expression score (GES) was constructed for differentially expressed genes to assess their diagnostic value as biomarkers. In SCZ patients, there were higher expression levels of CREB5, PPP3R1 and PPP1CB (P < 0.05) than in controls. Furthermore, DUSP1 and MAPK13 downregulated in undifferentiated SCZ and acute schizophrenia-like psychotic disorder (P < 0.05), PPP3R1 expression upregulated in paranoid SCZ, undifferentiated SCZ and acute schizophrenia-like psychotic disorder (P < 0.01), and CREB5 exclusively upregulated in paranoid SCZ (P = 0.001), respectively. The risk of SCZ was nonlinearly correlated with DUSP1, GNG10, GNG7, PRKACA, CREB5, PPP3R1 and PPP1CB (P < 0.05, P < 0.05). Meanwhile, incorporating these 7 genes into the GES improved the model's area under curve to 0.743, significantly enhancing the diagnostic discriminatory ability for SCZ. - Source: PubMed
Publication date: 2025/12/02
Zhou YuanZhu MengyaFan YaoWang FeifanMi SiqingShen ChongXue Yong - YAP is required for chondrogenesis and endochondral bone formation, but its effect on the hypertrophy and apoptosis of antler chondrocytes remains unclear. The present study revealed that YAP was abundantly expressed in antler chondrocytes. Inactivation of YAP restrained the hypertrophy of antler chondrocytes and facilitated chondrocyte apoptosis. Further analysis indicated that blockage of YAP induced the accumulation of cytosolic Ca by enhancing the stability of IP3R1/2 mRNA dependent on YTHDF2, that had been identified as a direct downstream target of YAP/TEAD. Meanwhile, attenuation of YAP activated the cytosolic Ca-mediated PPP3R1/NFATC pathway and then brought about the elevation of mitochondrial Ca via NFATC-targeted MCU. In antler chondrocytes, inactivation of YAP disrupted the mitochondrial morphology, diminished the ATP content and lowered the mitochondrial membrane potential, but these effects were neutralized by the blockage of MCU. Moreover, inhibition of YAP promoted the leakage of mtROS from dysfunctional mitochondria into the cytosol through opening the mitochondrial permeability transition pore, resulting in intracellular ROS accumulation and lipid peroxidation. Addition of ROS scavenger rescued the defective differentiation of antler chondrocytes and protected chondrocytes against apoptosis under the context of YAP inactivation. Collectively, YAP regulated the hypertrophy and apoptosis of antler chondrocytes through maintaining Ca homeostasis and mitochondrial function. - Source: PubMed
Publication date: 2025/09/14
Li Bai-YuYang Zhan-QingXing Yin-FeiZhang Qiao-LingWang Chen-HaoYue Zhan-PengGuo Bin - Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) accumulation, autophagic lysosomal pathway (ALP) dysfunction, mitochondrial abnormalities, and neuroinflammation. Physical exercise (PE) protects against AD, but its molecular mechanisms remain unclear. We hypothesize that PE-mediated upregulation of REV-ERBα and TFEB pathways mitigates AD-related dysfunctions. Acute effects of FK506, a calcineurin inhibitor, were assessed as a TFEB suppressor in mice subjected to aerobic exercise. Chronic treadmill training (8 weeks, 4 sessions/week) was performed in APP/PS1 mice to evaluate hippocampal adaptations through functional tests, imaging, and molecular analyses. Acute FK506 administration inhibited Ppp3ca and Ppp3r1 expression without altering Tfeb levels. Chronic PE improved aerobic capacity, strength, coordination, and memory, promoted neuronal survival, and decreased Aβ levels in APP mice. It also elevated REV-ERBα protein and Nr1 d1 expression in wild-type and APP mice, increased ALP activity, and reduced abnormal mitochondria in the hippocampus of APP mice. A positive correlation between REV-ERBα and Nr1 d1 levels was observed in the 2-min NOR test. Public RNA-seq data revealed lower NR1D1 mRNA in extracellular vesicles from the human frontal cortex of AD patients compared to controls. PE prevents cognitive decline in APP/PS1 mice, enhancing memory, physical performance, and hippocampal health. These benefits are associated with ALP activation, mitochondrial improvements, and reduced neuroinflammation. REV-ERBα may mediate these protective effects, but further studies using pharmacological and genetic models are needed to confirm its role. - Source: PubMed
Publication date: 2025/05/31
Morais Gustavo Paroschide Sousa Neto Ivo VieiraVeras Allice Santos CruzTeixeira Giovana RampazzoParoschi Luciana OliveiraPinto Ana PaulaDos Santos Jonathas RodrigoAlberici Luciane CarlaCintra Dennys Esper CorrêaPauli José RodrigoMorelli Ana PaulaRopelle Eduardo Rocheteda Silva Adelino Sanchez Ramos