CBL & PLCG1 Protein Protein Interaction Antibody Pair
- Known as:
- CBL & PLCG1 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0545
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CBL & PLCG1 Protein Interaction Antibody Pair
Related genes to: CBL & PLCG1 Protein Protein Interaction Antibody Pair
- Gene:
- PLCG1 NIH gene
- Name:
- phospholipase C gamma 1
- Previous symbol:
- PLC1
- Synonyms:
- PLC148, PLC-II, PLCgamma1, NCKAP3
- Chromosome:
- 20q12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-31
- Date modifiied:
- 2016-10-05
Related products to: CBL & PLCG1 Protein Protein Interaction Antibody Pair
Related articles to: CBL & PLCG1 Protein Protein Interaction Antibody Pair
- The gut-joint axis has been increasingly implicated in osteoarthritis (OA), yet the causal contribution of specific gut microbes and their downstream molecular mechanisms remain unclear. We employed a multi-stage, two-sample Mendelian randomization (MR) framework. This approach utilized summary-level data from large-scale genome-wide association studies (GWAS) for gut microbiota, plasma proteins, and OA. The analysis involved three steps: (1) identifying gut microbial taxa with potential causal associations with OA risk; (2) screening of pyroptosis-related proteins using pQTL data; and (3) performing mediation analysis to evaluate potential intermediate mechanisms. We also performed transcriptomic analysis of human cartilage and in vitro experiments in chondrocytes to support the biological relevance of our findings. Our MR analysis identified Gordonibacter pamelaeae as a suggestive microbial taxon inversely associated with OA risk. Among 11 candidate pyroptosis-related proteins, only Phospholipase C Gamma 1 (PLCG1) showed a significant inverse association with OA. MR analysis further suggested that G. pamelaeae was positively associated with genetically predicted PLCG1 levels. Mediation analysis indicated that PLCG1 partially mediated the association between G. pamelaeae and OA. Consistent with these findings, PLCG1 mRNA levels were reduced in human OA cartilage. Furthermore, our in vitro experiments demonstrated that PLCG1 knockdown enhanced IL-1β-induced inflammatory and pyroptotic responses in chondrocytes. This study suggests a potential link involving gut microbiota and OA through PLCG1-related signaling. PLCG1 may act as a context-dependent regulator that limits excessive inflammatory responses under stress conditions. These findings refine the current understanding of the gut-joint axis and may help identify potential targets for OA intervention. - Source: PubMed
Publication date: 2026/07/03
Li ShengkunZhong ShaoziZeng Chun - 1. Calcium (Ca) is essential for avian embryonic bone mineralisation, yet its metabolic dynamics during duck embryogenesis remain unclear. This study investigated Ca mobilisation in Muscovy duck embryos.2. Eggshell (ES) and yolk samples were collected from embryonic day (ED) 16 to ED31 for analysis of ES physical properties (thickness, strength, mass ratio) and Ca levels. Serum, yolk sac membrane (YSM) and liver tissues were collected from ED16 to the day of hatch (DOH) to assess serum biochemical parameters and relative mRNA expression of genes associated with Ca transport (, , ) and absorption (, , ).3. Results showed ES quality and Ca levels decreased ( < 0.01) linearly with increasing incubation days. Yolk Ca levels decreased ( < 0.01) linearly and quadratically, reaching a minimum on ED25. Serum Ca levels and alkaline phosphatase (ALP) activity increased ( < 0.01) linearly and quadratically during ED16-DOH and achieved a plateau during ED28-DOH. Expression of Ca-related genes in YSM and liver increased quadratically ( < 0.01), peaking during ED25-28.4. In conclusion, ES quality declined with reduced Ca levels during embryogenesis. Concurrently, yolk Ca levels, along with serum Ca and ALP levels, increased significantly during ED25-28, indicating peak embryonic Ca mobilisation during this period. Additionally, relative mRNA expression of Ca mobilisation-related genes in the YSM and liver exhibited a similar increasing trend. This suggested enhanced Ca mobilisation during this phase to support bone mineralisation and growth in duck embryos. - Source: PubMed
Publication date: 2026/06/24
Wang XRen YHu QWu QSun GChen HLin JLiu SWang WQin JZhu Y - Understanding how genetic variants influence disease risk through molecular mechanisms remains a central challenge in complex disease genetics. Nonsyndromic orofacial clefts (OFCs) exemplify this challenge, with most risk loci residing in non-coding regions. We hypothesized that common genetic variants influence OFC risk by modulating DNA methylation at regulatory elements through methylation quantitative trait loci (meQTLs). We analyzed 10 OFC-associated SNPs against genome-wide DNA methylation profiles in 409 cases and 456 controls, identifying 23 potential meQTLs. Findings were validated using 358 cleft-discordant sibling pairs with MethyLight assays. We performed formal mediation analysis, genotype-tissue interaction and cross-referenced with the mQTL Database to assess developmental timing. Nine meQTLs were validated, including rs987525 (8q24)-cg16561172 (MYC) (P = 9.6 × 10⁻⁶), which mapped to a mesendoderm-active enhancer upstream of MYC. Genotype × tissue interaction confirmed tissue-specificity (P = 1.00 × 10), with stronger effects in oral-derived tissue (saliva). Additional validated SNP-CpG associations involved MAFB-PLCG1, NOG-PPM1E, FOXE1-FRZB, and SPRY2-LGR4. While effect sizes correlated between tissues (r = 0.81), formal mediation analysis indicated individual CpG sites do not fully mediate SNP-phenotype relationships, suggesting coordinated epigenetic mechanisms. Most associations showed peak effects during childhood, while 8q24 showed unique adult-specific patterns. We identified genetic variants influencing methylation at craniofacial regulatory elements, and provided a mechanistic link for a major risk locus, 8q24, with tissue-specific effects in saliva. While individual CpG sites did not fully mediate the genetic risk, our findings identified specific regulatory regions where coordinated epigenetic changes may contribute to OFC susceptibility. - Source: PubMed
Publication date: 2026/06/23
Petrin A LMachado-Paula L AKeen H LHovey LDoolittle BDunlay LAwotoye WXie X JZeng EButali AMarazita M LMurray J CMoreno-Uribe L M - Chronic kidney disease (CKD) significantly increases the risk of coronary artery disease (CAD), but the causal plasma proteins linking these conditions are poorly understood. This study aimed to identify genetically validated plasma biomarkers and therapeutic targets for this cardiorenal link. - Source: PubMed
Publication date: 2026/06/16
Huang HaiQuanLiu WenkangYan YaNanCao JuanWang JiePengFang ChaoYi - Phospholipase C-γ1 (PLC-γ1) signaling is required for mesenchymal chemotaxis, but is it sufficient to bias motility? PLC-γ1 enzyme activity is basally autoinhibited, and light-controlled membrane recruitment of wild-type PLC-γ1 (OptoPLC-γ1) in Plcg1-null fibroblasts does not trigger lipid hydrolysis, complicating efforts to isolate its contribution. Utilizing cancer-associated mutations to investigate the regulatory logic of PLC-γ1, we demonstrate that a hallmark of enzyme activity, phosphorylated Tyr783, is not a proxy for activity level, but is rather a marker of dysregulated autoinhibition. Accordingly, OptoPLC-γ1 with a deregulating mutation (P867R, S345F, or D1165H) exhibits elevated phosphorylation, and membrane localization of such is sufficient to activate substrate hydrolysis and concomitant motility responses. In particular, local recruitment of OptoPLC-γ1 S345F polarizes cell motility and migration on demand. This response is spatially dose-sensitive and only partially reduced by blocking canonical PLC-γ1 signaling, yet is lipase-dependent. Our findings reframe the interpretation of PLC-γ1 regulation and demonstrate that local activation of PLC-γ1 is sufficient to direct cell motility. - Source: PubMed
Publication date: 2026/05/05
Appalabhotla RavikanthSiesser Priscila FTruscott HarrisonHajicek NicoleSondek JohnBear James EHaugh Jason M