Ask about this productRelated genes to: PTRF antibody
- Gene:
- CAVIN1 NIH gene
- Name:
- caveolae associated protein 1
- Previous symbol:
- PTRF
- Synonyms:
- cavin-1, CGL4
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-21
- Date modifiied:
- 2017-03-24
Related products to: PTRF antibody
Related articles to: PTRF antibody
- 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 - Backfat thickness, a key selection trait in pig-breeding programmes, has traditionally been measured as a homogeneous layer. However, backfat is anatomically structured into three distinct layers, and each layer likely contributes differently to carcass quality. In addition, previous studies have shown that the deposition of the third layer of backfat is phenotypically correlated with intramuscular fat (IMF). Therefore, targeted selection for specific backfat layers, particularly the third layer, represents a potential strategy to increase IMF content while maintaining a high lean meat percentage. However, the genetic architecture of these distinct porcine backfat layers remains poorly understood. The aim of this study was to estimate the genetic parameters and identify key candidate genes underlying the three backfat layers. We collected B-mode ultrasound images from 561 Landrace pigs to measure individual layer thickness, followed by DNA extraction, genotyping, genetic parameter estimation, and a genome-wide association study (GWAS). Our measurements showed that the first layer of backfat (FBF) is the thickest, followed by the second (SBF) and the third (TBF) layers. Genetic parameter estimation yielded heritability estimates of 0.37, 0.42, 0.38, 0.34, 0.32, 0.24, and 0.21 for total backfat (BF), FBF, FBF/BF, SBF, SBF/BF, TBF, and TBF/BF, respectively. Through integrated analysis of GWAS, Bayesian fine-mapping, and gene annotation, we identified 15 non-redundant candidate genes associated with different backfat layers. These included two genes (SOAT1 and ACBD6) shared by BF and SBF, LPL for BF and FBF, and CAND1 for TBF and TBF/BF. Additionally, SERPINA12 and SERPINA6 were associated with BF; PRKAG1 and PRDM16 with FBF; EPRS1 and SLC39A10 with FBF/BF; PTGES and CRAT with SBF; and ACLY, CAVIN1, and PDZRN3 with SBF/BF. Our results indicate that each layer is governed by a distinct set of genes, which advances our understanding of the genetic basis of backfat layers in pigs. - Source: PubMed
Publication date: 2026/01/20
Meng ZLiu YYang WWang JLi P HHuang R HWu W J - Metastatic triple-negative breast cancer (TNBC) is highly aggressive and lacks targeted therapies. Circulating tumor cells (CTC) are invaluable for monitoring metastatic tumor progression and treatment response but are difficult to capture because of their rarity and heterogeneity. Surface-based staining for live CTCs is essential to preserve RNA quality in single cells, but current markers tend to perform poorly on more mesenchymal tumor cells such as TNBCs. To enhance live TNBC CTC detection, we developed a workflow for live CTC capture and single-cell RNA sequencing (scRNA-seq). Using a mouse model of metastatic TNBC, we identified four new CTC surface markers, AHNAK2, CAVIN1, ODR4, and TRIML2, which specifically stain tumor cells. Combining antibodies against these markers improved CTC detection rates in multiple TNBC mouse models and patient samples. Also, combining these new markers with traditional CTC surface markers enhanced detection sensitivity, achieving the highest CTC coverage. This approach identifies diverse CTC populations, while preserving RNA quality for scRNA-seq, which is essential for understanding and therapeutically targeting metastatic breast cancer. The use of these newly identified CTC markers significantly enhances both detection and live capture of CTCs, paving the way for more effective use of liquid biopsy to monitor patient prognosis and treatment response in clinical settings. - Source: PubMed
Lege Bree MPatel Khushali JPanici BrendanGong PingLewis Michael TEllis Matthew JCheng Chonghui - Trans-endothelial transport of nanoparticles remains poorly characterized in live organisms. The zebrafish is a well-established model for direct imaging; however, standardized controls have not been consistently applied across studies. Here, we developed a standardized protocol to assess nanoparticle trans-endothelial trafficking in live zebrafish. We identified 2000 kDa dextran as an optimal coinjection control for standardizing microinjections and quantifying nanoparticle transport in a systematic, unbiased manner. Using the standardized protocol, we profiled early physiological trans-endothelial transport pathways in zebrafish embryos using dextran solutes as extravasation markers, showing that steady-state solute extravasation is characterized by paracellular routes selective for solutes <15 nm in diameter, dynamin-mediated endocytosis, and low basal macropinocytosis. We assessed the extravasation of 3, 7, 32, 47, 81, and 109 nm polyethylene glycol (PEG)-based nanoparticles using this protocol. Using a pretreatment protocol with chemical inhibitors, we demonstrate that <7 nm PEG-based hyperbranched polymer (HBP) nanoparticles undergo rapid paracellular extravasation, 32 to 81 nm PEG-based micelles adopt dynamin-dependent and macropinocytic trafficking over paracellular transport, and 109 nm PEG-based micelles extravasate primarily via macropinocytic trafficking. We characterized the emergence of vascular caveolae up to 17 days postfertilization with a knock-in zebrafish line. Using / double knockout zebrafish and tumor-bearing Cavin1 null mice, we showed that caveolae do not contribute to the transvascular transport of these PEG-based nanoparticles. This work demonstrates the rigor of the standardized protocol for assessing trans-endothelial transport in the live zebrafish and provides fundamental cell biology insight into the behavior of PEG-based nanoparticles. - Source: PubMed
Publication date: 2026/01/14
Lim Ye-WheenBell Craig AFletcher Nicholas LCondon Nicholas DAkhter Dewan TRae JamesFerguson CharlesMartel NickHumphries JamesLo Harriet PWu YepingHouston Zachary HLagendijk Anne KHall Thomas EThurecht Kristofer JParton Robert G - Pancreatic cancer is a highly aggressive malignancy with serious threat to human health and survival. Cavin1, a caveolin-associated protein, has recently been identified as a differentially expressed gene linked to lipid droplet formation, suggesting its potential involvement in pancreatic cancer biology. However, the significance and underlying mechanisms of Cavin1 in the progression of pancreatic cancer remain poorly understood. In this present study, we demonstrated that Cavin1 expression was significantly elevated in pancreatic cancer, its knockdown significantly inhibited cell proliferation, and its suppression enhanced apoptotic activity in pancreatic cancer cells. In addition, inhibition of Cavin1 impaired lipid metabolism, and silencing of Cavin1 activated the adenosine 5'-monophosphate-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) signaling pathway. In conclusion, Cavin1 depletion was found to impair tumor cell growth by inhibiting proliferation and lipid metabolism while promoting apoptosis, supporting Cavin1 as a potential therapeutic target for pancreatic cancer management. - Source: PubMed
Publication date: 2026/01/05
Liu WeiWang LiguoZhou YiZhu Song