CAPZA1
- Known as:
- CAPZA1
- Catalog number:
- GTX15735
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CAPZA1
Related genes to: CAPZA1
- Gene:
- CAPZA1 NIH gene
- Name:
- capping actin protein of muscle Z-line subunit alpha 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-26
- Date modifiied:
- 2018-04-23
Related products to: CAPZA1
anti-CAPZA1anti-CAPZA1anti-CAPZA1Anti-CAPZA1 AntibodyAnti-CAPZA1 Antibodyanti-CAPZA1 type: Primary antibodies host: MouseBeta-actinin subunit I,CapZ 36_32,CAPZA1,Chicken,F-actin-capping protein subunit alpha-1,Gallus gallusBos taurus,Bovine,CapZ alpha-1,CAPZA1,F-actin-capping protein subunit alpha-1Bovine capping protein (actin filament) muscle Z-line, alpha 1 (CAPZA1) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine F-actin-capping protein subunit alpha-1(CAPZA1) ELISA kitBovine F-actin-capping protein subunit alpha-1(CAPZA1) ELISA kit SpeciesBovineCappa1,CapZ alpha-1,Capza1,F-actin-capping protein subunit alpha-1,Mouse,Mus musculusCAPS2 Gene calcyphosine 2CapZ alpha-1,CAPZA1,F-actin-capping protein subunit alpha-1,Homo sapiens,HumanCapZ alpha-1,Capza1,F-actin-capping protein subunit alpha-1,Rat,Rattus norvegicus Related articles to: CAPZA1
- Intervertebral disc degeneration (IVDD) is a leading cause of low back pain, characterized by the progressive senescence of nucleus pulposus cells (NPCs) and extracellular matrix (ECM) catabolism. Although bulk autophagy has been implicated in the pathogenesis of IVDD, the specific contribution of selective autophagy to NPC fate remains largely unexplored. Here, we identify NDP52, a selective autophagy receptor, as a critical regulator of NPC homeostasis. NDP52 expression was significantly downregulated in degenerative NP tissues from humans, aged mice and needle puncture-induced IVDD models. NDP52 deficiency promoted NPC senescence, characterized by cell cycle arrest, senescence-associated secretory phenotype (SASP) factor secretion and reactive oxygen species (ROS) accumulation, ultimately leading to impaired ECM homeostasis, whereas NDP52 overexpression exerted opposite effects. In vivo, NDP52 knockout mice exhibited more severe disc degeneration and heightened pain sensitivity than wild-type controls. Deletion of the ZF2 domain abolished the protective effects of NDP52 in NPCs, indicating that its selective autophagy function is required for maintaining NPC homeostasis. Integrated proteomic and IP-MS analyses identified CAPZA1 as a candidate substrate of NDP52. Subsequent biochemical analyses demonstrated that NDP52 promotes the autophagic degradation of CAPZA1, an F-actin capping protein, through its ZF2 domain. Loss of NDP52 resulted in CAPZA1 accumulation, which was accompanied by aberrant ROS accumulation and activation of p53/Rb-dependent cell cycle arrest and NF-κB-mediated SASP signaling. CAPZA1 knockdown rescued the senescent and degenerative phenotypes caused by NDP52 deficiency. These findings identify the NDP52-CAPZA1 selective autophagy axis as a key protective mechanism against IVDD and highlight potential therapeutic targets for this prevalent degenerative disorder. - Source: PubMed
Publication date: 2026/04/28
Yao Ge-LiangXie Xin-ShengWang Shi-JiangJiang Hao-XinXiong XuDu Liu-XueLiu Jia-MingSong Hong-HaiLiu Zhi-Li - Observational studies suggest an association between Coronavirus Disease 2019 (COVID-19) and polymyositis (PM), but causal inference s limited by confounding. This study adopted a multilevel exploratory framework to investigate potential relationships. We used two-sample Mendelian randomization (MR) to assess the causal effect of severe COVID-19 on PM, multi-omic analyses to screen for potential mediators, and retrospectively compared hematological profiles between severe and non-sever COVID-19 cases. - Source: PubMed
Publication date: 2026/04/09
Chen MiaomiaoLi HongmeiTong XiaZhang Xin - BACKGROUND: The development of pulmonary hypertension (PH) is a serious complication of chronic obstructive pulmonary disease (COPD). Despite advances in characterizing pulmonary vascular remodeling in COPD-PH, the lack of targeted therapies limits the routine use of gold-standard invasive diagnostics, highlighting the need for novel biomarkers. The pulmonary vascular endothelium is central to the pathogenesis of both PH and COPD. Since most endothelium-derived modulators of vascular tone and remodeling are targets of endothelial-enriched microRNA-126 (miR-126), a master vascular regulator that is suppressed in COPD, these and related ‘angiocentric molecules’ may be promising biomarkers for COPD-PH. RESEARCH GOAL: To identify angiocentric proteins elevated in individuals with suspected COPD-PH, defined by a pulmonary artery-to-aorta ratio (PA/A) > 1 on thoracic CT, and to evaluate if they are significantly associated with the severity of airflow limitation (FEV₁). STUDY DESIGN: We analyzed plasma proteomic profiles from 1,056 COPDGene Phase-1 participants. Using PA/A > 1 as the outcome, we identified differentially abundant angiocentric proteins. We then assessed the abundance of angiocentric proteins in those with severe airflow obstruction (FEV₁ <50% predicted) among both the COPDGene Phase-1 participants and 188 SPIROMICS Visit-1 participants, and validated the findings in an independent cohort of 363 COPDGene Phase-2 participants. Mediation analyses of multi-omic data examined the relationships between specific miR-126-3p and -p strands levels, their target mRNA and protein levels, and the severity of airflow obstruction. RESULTS: Seventeen angiocentric proteins were increased in participants with PA/A > 1, with interleukin-1 receptor-like 1 (IL1RL1) and platelet-derived growth factor B (PDGFB) showing the most significant elevations. Among those with FEV₁ <50% predicted, eleven angiocentric proteins were increased, including IL1RL1, angiopoietin-2, and peroxiredoxin-5. Mediation analyses supported a contribution of reduced miR-126 levels to lower FEV₁ via select angiocentric molecules, including the direct miR-126 target selenoprotein T. Additionally, LINC01506 and CAPZA1 had a mediation effect on multiple clinical outcomes, including FEV₁, DLCO, and hematocrit. CONCLUSION: In addition to their role in pulmonary vascular remodeling, miR-126–regulated angiocentric proteins are also linked to airflow limitation, highlighting their potential as candidate biomarkers for COPD-associated pulmonary hypertension. - Source: PubMed
Publication date: 2026/03/28
Goel KhushbooOrmesher RyenPratte Katherine AWang YueNishino KoichiHersh Craig PKechris KaterinaBowler Russell PPetrache Irina - To investigate the genetic and molecular role of CAPZA1 in asthenozoospermia and its impact on sperm motility and flagellar integrity. - Source: PubMed
Publication date: 2026/03/04
Lu HuiLi GuoxuanHu JiajiaRuan HailingZhao LiqiangLi YejuanWang Anguo - Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive and prevalent cancers in China, a deeper understanding at the molecular level is the cornerstone for advancing precision oncology in ESCC. This study aims to investigate the role of CAPZA1 in ESCC progression. Based on our previous whole genome sequencing (WGS) and whole exome sequencing (WES) data indicating frequent copy number loss of CAPZA1 in ESCC, as well as the presence of a specific single nucleotide polymorphism (SNP, rs373245753 T>G) in its 3'UTR via the dbSNP database (https://www.ncbi.nlm.nih.gov/snp/), we sought to determine the functional and mechanistic impact of CAPZA1 genotypes on ESCC cell behavior. - Source: PubMed
Kang NanOu YunweiGuo ShichaoChen JieLi DanZhan Qimin