Mouse polyclonal to PRKCDBP, Host Mouse
- Known as:
- Mouse pab PRKCDBP, Host Mouse
- Catalog number:
- YF-PA26803
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal PRKCDBP Host
Related genes to: Mouse polyclonal to PRKCDBP, Host Mouse
- Gene:
- CAVIN3 NIH gene
- Name:
- caveolae associated protein 3
- Previous symbol:
- PRKCDBP
- Synonyms:
- SRBC, HSRBC, MGC20400, cavin-3
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-15
- Date modifiied:
- 2017-03-24
Related products to: Mouse polyclonal to PRKCDBP, Host Mouse
Related articles to: Mouse polyclonal to PRKCDBP, Host Mouse
- This study aims to investigate the expression of CAVIN3 in cervical cancer, its effect on radiotherapy outcomes, and its potential molecular mechanisms. - Source: PubMed
Publication date: 2026/08/08
Ye YingFu ZhichaoWang XinpengDeng ShilongCai LvjuanFeng JingWang Fengmei - Adipogenic differentiation is essential for adipose tissue development, fat deposition, and metabolic regulation in livestock, but the role of RNA-binding proteins in sheep preadipocyte differentiation remains unclear. This study investigated whether Quaking () regulates sheep preadipocyte adipogenesis and explored its downstream regulatory mechanism. expression was examined in sheep adipose tissues, and knockdown was performed in sheep preadipocytes. Adipogenic marker expression, lipid accumulation, glucose consumption, Oxford Nanopore Technologies (ONT) full-length transcriptome sequencing, RNA immunoprecipitation coupled with quantitative real-time PCR (RIP-qPCR), actinomycin D assay, caveolae-associated protein 3 () knockdown, and simultaneous and knockdown were used to evaluate the function and mechanism of . was expressed in different sheep adipose tissues, with relatively higher expression in tail fat. knockdown reduced adipogenic marker expression, Oil Red O staining, and glucose consumption after adipogenic induction. ONT full-length transcriptome sequencing identified as a markedly upregulated candidate downstream target after knockdown. RIP-qPCR showed enrichment of mRNA in QKI immunoprecipitates, and actinomycin D assays indicated that knockdown delayed mRNA degradation. knockdown enhanced adipogenic marker expression, Oil Red O staining, and glucose consumption. Simultaneous and knockdown increased adiponectin, fatty-acid-binding protein 4, and peroxisome proliferator-activated receptor gamma mRNA abundance and Oil Red O staining relative to the matched control, whereas glucose consumption was not significantly different. These findings suggest that promotes sheep preadipocyte differentiation, at least in part, by reducing mRNA stability, providing insight into RNA-binding protein-mediated regulation of livestock adipogenesis. - Source: PubMed
Publication date: 2026/08/06
Li ZichengXu ChangsongShan BokangWang YuanQin WangyangXia LeiQiao LiyingLiu WenzhongPan Yangyang - Cavins, in concert with caveolins, orchestrate the formation and function of caveolae-specialized invaginations of the plasma membrane involved in mechanotransduction, lipid homeostasis, and cell signaling. The Cavin family comprises four members: Cavins 1-3, which are broadly expressed, and Cavin4, which is muscle-specific. Disruption of Cavin function via genetic mutations, epigenetic silencing, or altered expression is linked to a spectrum of caveolae-related disorders, including lipodystrophy, muscular dystrophies, insulin resistance, and cancer. This review offers a comprehensive analysis of the physiological roles, pathophysiological implications, and therapeutic potential of cavins, with emphasis on their involvement in cancer, metabolic diseases, and muscle disorders, highlighting their value as biomarkers and molecular targets in precision medicine. Specifically, Cavin1 serves as the central structural and functional scaffold of caveolae, linking mechanoprotection, lipid metabolism, and ribosomal RNA transcription to cellular stress adaptation and disease pathogenesis, whereas Cavin2 modulates caveolae morphology and signaling, with emerging roles in insulin sensitivity and inflammatory regulation. Cavin3, in turn, is considered a dynamic regulator of caveolae turnover and signal integration, linking caveolar function to cell signaling, DNA damage responses, and tumor suppression. Finally, Cavin4 plays a critical role in muscle-specific caveolae organization, mechanotransduction, and hypertrophic signaling. In the context of tumorigenesis, cavins together represent promising therapeutic targets due to their capacity to induce apoptosis, inhibit cancer cell migration and invasion, and modulate inflammatory responses; however, their roles appear to be context-dependent, with expression patterns and functional outcomes varying across tissue types. - Source: PubMed
Publication date: 2026/02/10
Osman YoussefAkimbekov Nuraly SEl-Zayat Emad MHassan NourhanDigel Ilya - Cavin family proteins alter the invasiveness of tumor cells. However, research on the pathogenesis of Cavins in tumors is lacking. To address this knowledge-gap, we conducted a systematic analysis about the mechanism of action of Cavins in cancer. We evaluated the diagnostic value of Cavin-3 and its potential as a new therapeutic target for lung squamous cell carcinoma (LUSC). Bioinformatic analysis showed that Cavin-3 can inhibit LUSC tumor cells by regulating the expression of EREG and IL1A, thereby activating the MAPK pathway to promote the release of tumor necrosis factor (TNF) and other inflammatory factors. Moreover, in vitro experiments have shown that Cavin-3 may promote the expression of inflammatory factors by regulating the MAPK signaling pathway, thereby killing tumor cells and inhibiting tumor proliferation. - Source: PubMed
Publication date: 2025/11/26
Xu XiaoyanNie YonghongXu JiatuoJiang Rilei - Cervical cancer progression is intricately linked to dysregulated cell death pathways, particularly PANoptosis, a coordinated form of programmed cell death. However, prognostic biomarkers and immunological implications of PANoptosis-related genes (PRGs) in cervical cancer remain underexplored. - Source: PubMed
Publication date: 2025/11/22
Tong YuehongDeng WeiXu LiliLi YaoZhang Keke