MCPIP1 antibody
- Known as:
- MCPIP1 (anti-)
- Catalog number:
- orb100486
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- MCPIP1 antibody
Related genes to: MCPIP1 antibody
- Gene:
- ZC3H12A NIH gene
- Name:
- zinc finger CCCH-type containing 12A
- Previous symbol:
- -
- Synonyms:
- FLJ23231, MCPIP1
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-03
- Date modifiied:
- 2014-11-19
Related products to: MCPIP1 antibody
Related articles to: MCPIP1 antibody
- Hepatic ischemia-reperfusion injury (HIRI) is clinically linked to post-transplant complications, yet the pathogenic role of programmed cell death (PCD) patterns in this process remains poorly delineated. This study aimed to investigate the diversity of programmed cell death (PCD) patterns underlying HIRI, with a focus on mechanistically dissecting macrophage-hepatocyte crosstalk mediated by the THBS1-CD47 axis. - Source: PubMed
Publication date: 2026/05/19
Xie ManlingZhang ChangquanZhu LirongPei YongfengLiang ChunyanFu LixinLi HaibinLan LiugenWen NingWu JihuaSun Xuyong - Compared with commercial laying hens, indigenous chicken breeds generally exhibit lower reproductive performance. This study aims to elucidate the impact of abdominal fat deposition on the reproductive performance of indigenous chickens, providing a theoretical basis for the breeding of high-yielding chickens. - Source: PubMed
Publication date: 2026/04/28
Yu HailiangWu LeiWang HaoYuan ChenxuShi JiajiaJi QianyunBai YaruZhu XiaoliGuo LipingZhang ChengChen Xingyong - Candida albicans (C. albicans) is the leading cause of systemic candidiasis in immunocompromised individuals and is associated with substantial mortality. As current antifungal therapies are limited by suboptimal efficacy and the emergence of resistance, improved understanding of host-pathogen interactions that govern antifungal immunity is essential for identifying new therapeutic strategies. Here, we identify MCPIP1 as a host factor that negatively regulates antifungal immune responses during lethal C. albicans infection. Integrative bioinformatic analyses of transcriptomic profiles from human peripheral blood mononuclear cells (PBMCs) exposed to C. albicans identified MCPIP1 as a macrophage-associated gene closely linked to infection-induced immune remodeling. Functional validation using in vivo and in vitro models demonstrated that MCPIP1 expression was markedly induced following systemic C. albicans infection and that MCPIP1 impaired host antifungal defenses. In a murine model of systemic candidiasis, administration of recombinant MCPIP1 exacerbated disease severity, leading to increased fungal burdens, aggravated kidney injury, and reduced host survival. Consistently, MCPIP1 suppressed macrophage-mediated phagocytosis and killing of C. albicans in vitro, indicating a direct role in regulating host-pathogen interactions at the cellular level. Mechanistically, MCPIP1 attenuated macrophage antifungal activity by suppressing p38 MAPK and ERK1/2 signaling pathways, whereas activation of these pathways restored antifungal immune function and mitigated MCPIP1-mediated immunosuppression. Together, these findings identify MCPIP1 as a key host regulator that shapes antifungal immunity during systemic C. albicans infection and highlight MCPIP1 as a potential immunomodulatory target for the treatment of invasive fungal disease. - Source: PubMed
Publication date: 2026/04/30
Gao XuepingTan LinDing HaoYu RenlinLiu YaoTan WangHan XinyuanHe YueyueLai XiaofeiCao Ju - Monocyte chemoattractant protein-induced protein 1 (MCPIP1), encoded by ZC3H12A, is a negative regulator of inflammation and tumorigenesis. While its role has been implicated in various cancers, the function of MCPIP1 in hepatocellular carcinoma (HCC) remains poorly understood. This study explored the contribution of hepatocyte-specific MCPIP1 loss to HCC pathogenesis, highlighting its role in overcoming the inherent tumor resistance observed in female mice. - Source: PubMed
Publication date: 2026/01/29
Kwapisz OliwiaMarona PaulinaGorka JudytaMyrczek RafałGonzalez-Sanchez EsterBertran EstherKotlinowski JerzyGłuc MaciejAlay AniaPydyn NataliaKujdowicz MonikaRamos EmilioFabregat IsabelMiekus Katarzyna - CAR-T cell therapies are revolutionizing the treatment of refractory or relapsed hematological malignancies, but many patients do not achieve durable responses, and these therapies remain ineffective against solid tumors. Therapeutic failure is closely associated with a poor persistence of CAR-T cells in patients, highlighting the need to identify strategies promoting in vivo expansion. Although numerous gene-editing strategies have been proposed, comparative studies to identify the most effective ones are still lacking. Here, using a focused CRISPR-knockout library targeting 50 selected gene candidates, we developed a competitive screening that revealed ZC3H12A, SOCS1, PTPN2, and CDKN2A as the most robust targets to improve persistence of EGFR CAR-T cells in human lung tumor-bearing mice. Surprisingly, disruption of other genes previously reported to improve CAR-T cell efficacy in other preclinical models-MED12, PRDM1, and BATF-had a detrimental effect in this context. These results suggest that some gene-editing strategies can yield beneficial, neutral, or even deleterious effects on CAR-T cell persistence, depending on specific conditions. Altogether, these findings highlight the importance of performing context-specific evaluations of genetic modifications to accelerate the clinical translation of the most promising editing strategies for optimizing CAR-T cell therapies. - Source: PubMed
Publication date: 2026/04/04
Fumagalli MattiaAn DongjieSimula LucaCombe CamilleAziez LisaSimoni YannickAlves-Guerra Marie-ClotildeValentini AndreaMarchais MaudeVermare AnaïsMoraly JosquinManni SimonaQuadraccia Maria CeciliaQuintarelli ConcettaDe Angelis BiagioBercovici NadègeDonnadieu EmmanuelPendino Frédéric