CAPG, 1_348aa, Human, E.coli
- Known as:
- CAPG, 1_348aa, Human, E.coli
- Catalog number:
- ATGP0439
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- CAPG 1_348aa Human .coli
Ask about this productRelated genes to: CAPG, 1_348aa, Human, E.coli
- Gene:
- CAPG NIH gene
- Name:
- capping actin protein, gelsolin like
- Previous symbol:
- AFCP
- Synonyms:
- MCP
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-14
- Date modifiied:
- 2016-01-18
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
Related products to: CAPG, 1_348aa, Human, E.coli
Related articles to: CAPG, 1_348aa, Human, E.coli
- Breast cancer (BC) remains the leading cause of cancer-related death among women worldwide, with 2.26 million new cases and ∼685,000 deaths reported in 2020 (Globocan 2020). A major challenge in treating BC, particularly luminal subtypes, is the pronounced molecular heterogeneity both between patients and within individual tumours. This intratumoural diversity underlies many cases of therapy resistance and relapse. Here, we present a theranostic approach that integrates spatial proteomics and patient-derived tumoroids (PDTs) to guide personalized treatment in luminal BC. Formalin-fixed, paraffin-embedded (FFPE) tumour tissues from three patients were analyzed by MALDI mass spectrometry imaging (MSI) and spatially-resolved micro-proteomics, mapping distinct clonal subpopulations and their protein expression profiles. Proteomic pathway analysis revealed subclone-specific vulnerabilities that are not apparent from standard histopathology. We exploited these insights to design alternative combination therapies tailored to each tumour's molecular makeup. The efficacy of proteomics-guided regimens was then evaluated in vitro using PDTs established from the same patients, in direct comparison to conventional chemotherapy. Proteomic-informed treatments demonstrated significantly enhanced anti-tumour activity in the PDT models, yielding lower IC values and greater cell death than standard treatments. In several cases, PDTs exhibited resistance to conventional therapy, which was explained by the presence of proteomic resistance markers (such as EDIL3, CA12, PGK1, and CapG) in the corresponding tumour clones. These results underscore the potential of spatial proteomic profiling to expose actionable intratumoural heterogeneity and to inform more effective, clone-specific therapies. Our study highlights an innovative pipeline for luminal BC therapy guidance, combining MALDI MSI and PDT drug testing, and advocates for the integration of spatial proteomics into precision oncology to improve treatment outcomes. - Source: PubMed
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Lagache LaurineRaffo-Romero AntonellaDuhamel MarieZirem YanisVanseymortier MaireFournier IsabelleHajjaji NawaleSalzet Michel - The potential pathogenesis and reliable biomarkers of Bladder cancer (BC) remain to be explored. Ubiquitination plays a crucial role in BC progression, warranting the necessity to develop prognostic gene signatures. - Source: PubMed
Publication date: 2026/07/28
Li ZhibiaoYan TingHu ChuxianLu ZechaoZhang JiahaoWu XiujunChen YushuTang ZhichengZheng HanxiongHe ZhaohuiTang Fucai - Calcium phosphate graphene (CaPG) is a promising reinforcement for polymeric bone matrices, yet the impact of graphene oxide (GO) oxidation on CaPG chemistry and matrix performance remains unclear. Our previous work demonstrated that 5 wt% CaPG provides optimal mechanical and biological performance of poly (lactic-co-glycolic acid) (PLGA) matrix. The present study isolates GO oxidation as the sole variable while maintaining a fixed 5 wt% CaPG loading. CaPG was synthesized under three oxidation conditions: Low Phosphate-High Oxygen at 50 °C, High Phosphate-High Oxygen at 100 °C, and High Phosphate-Low Oxygen at 156 °C and incorporated into the PLGA microspheres. Our results have shown that oxidation state regulates oxygen functional group density, calcium phosphate incorporation, hydrophilicity, and hydration behavior, which collectively modulate mechanical properties and osteogenic activity of the matrix. These findings demonstrate that oxidation can serve as a key tunable factor that generates distinct physicochemical and biological profiles, establishing oxidation programming as a practical approach for creating adaptable CaPG-reinforced PLGA matrices for diverse bone regeneration needs. - Source: PubMed
Publication date: 2026/08/05
Hosseini Fatemeh SKan Ho-ManWhitfield TarajeArgyrou ChrysoulaSilva DilshanDeng ChenyunOrlando Jason DNair LakshmiSydlik Stefanie AMaye Peter FLo Kevin W-HLaurencin Cato T - Emerging evidence implicates intestinal barrier dysfunction and translocation of microbial factors as key drivers of post-myocardial infarction inflammation and cardiac remodeling, yet therapeutic strategies targeting the gut-heart axis remain underdeveloped. Here we demonstrate that ALY688, an adiponectin receptor agonist peptide, confers robust cardioprotection in rat myocardial ischemia-reperfusion (IR) injury through coordinated immunoregulatory programs in cardiac and intestinal tissues. ALY688 administration during ischemia or at reperfusion and subsequently daily for 28 days significantly preserved cardiac function with improved ejection fraction and fractional shortening, reduced infarct size, and decreased cardiac troponin-I levels. Mechanistic investigation revealed tissue-specific immune reprogramming: in the myocardium, ALY688 directly activated macrophages to secrete TGFβ1, which promoted regulatory T cell (Treg) differentiation from naïve CD4 + T cells as validated in macrophage-T cell co-culture systems. This macrophage-to-Treg axis suppressed inflammasome activation and IL-1β/IL-23/IL-6 signaling while enhancing anti-inflammatory macrophage polarization. Simultaneously, ALY688 strengthened intestinal barrier integrity through activation of the RORγt/IL-17 pathway, upregulating tight junction proteins (Claudin-1, ZO-1) and mucins (MUC19, MUC22), thereby limiting systemic spillover of bacterial endotoxin (LPS) and other microbial metabolites. Multi-omics profiling supported this dual-compartment mechanism: proteomics revealed modulation of immune regulatory (CAPG, CORO1A, MCAM) and cardioprotective (clusterin, NPPA) proteins, while metabolomics demonstrated attenuation by ALY688 of post-IR elevations in pathogenic gut-derived metabolites (anthranilic acid, imidazole propionate, linoleic acid derivatives). This study establishes adiponectin receptor activation as a multi-organ immunometabolic intervention that simultaneously resolves cardiac inflammation while protecting intestinal barrier function. These findings provide mechanistic insight for therapeutic strategies that target the gut-heart axis to address a major remaining unmet clinical need in ischemic heart disease. - Source: PubMed
Publication date: 2026/07/28
Tang JialingSung Hye KyoungLei YubinTeerawongsuwan SasipatRungsiwiwut RuttachukWannaiampikul SivapornChen JiaruiRidany IbrahimRichard VincentBorchers ChristophKim YoojungCho Ssang-GooCoquant GaranceCorr Sinéad CWu JunLi Ren-KeWang ChaoAbdul-Sater Ali ASweeney Gary - Administration of recombinant tissue plasminogen activator (rtPA) beyond 4.5 h after ischemic stroke exacerbates blood-brain barrier (BBB) disruption, leading to vasogenic cerebral edema and hemorrhage. However, current therapies remain ineffective. - Source: PubMed
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