Ask about this productRelated genes to: PHLDA1 antibody
- Gene:
- PHLDA1 NIH gene
- Name:
- pleckstrin homology like domain family A member 1
- Previous symbol:
- -
- Synonyms:
- TDAG51, DT1P1B11, PHRIP
- Chromosome:
- 12q15
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-19
- Date modifiied:
- 2016-01-27
Related products to: PHLDA1 antibody
Related articles to: PHLDA1 antibody
- Herpesviruses infect nearly all humans and have long been implicated in autoimmune and chronic diseases, yet their immune interactions with host proteins have not been systematically characterized at population scale. We profiled immunoglobulin G reactivities to >4,600 herpesvirus peptides and >15,000 human proteins using multiplexed protein display in two Mass General Brigham Biobank cohorts (discovery n=1,289; replication n=763), with longitudinal electronic health record follow-up. We identified and replicated 3,943 FDR-significant associations across 93 autoantigens, including previously uncharacterized viral-autoantigen axes, such as PHLDA1 and ZNF550. Eleven autoantigens were predicted by viral peptide reactivities with >85% accuracy in independent validation; some exhibited shared viral-host sequence homology, consistent with possible molecular mimicry. Integrating immune reactivities with incident disease outcomes revealed virus-specific network architectures: cytomegalovirus formed the largest multimorbid network, Epstein-Barr virus converged on pleiotropic autoimmune hubs, and herpes simplex viruses formed smaller, partially overlapping autoreactive networks. These findings define a herpesvirus-autoantigen-disease network atlas and prioritize candidate viral-host immune axes for mechanistic investigation. - Source: PubMed
Publication date: 2026/04/13
Lee SanghunPrince NicoleChen QingwenChen XueyingLu JunweiMendez Kevin MKelly Rachel SHecker JulianProkopenko DmitryMcGeachie Michael JSharma RinkuChen YuluAparicio AndreaGuo TaoLevy OferRattray Nicholas JwRattray ZahraLange ChristophLarman H BenjaminLasky-Su Jessica A - Deoxynivalenol (DON), a prevalent food-borne mycotoxin, increasingly recognized as a potent driver in the progression of chronic liver disease to cirrhosis and hepatocellular carcinoma (HCC); however, its systematic role is unclear. This study aims to decode the pathogenic networks of DON through an integrated multi-omics and toxicological framework. - Source: PubMed
Publication date: 2026/04/08
Fu YunfengYang SichengPan YatingYan RunweiDu FanZhou Xiaodong - Hypertrophic cardiomyopathy (HCM) is a common inherited cardiomyopathy characterized by ventricular hypertrophy, fibrosis, and increased risk of sudden cardiac death. However, the underlying molecular pathways contributing to its progression remain incompletely defined. PANoptosis, a newly defined inflammatory form of programmed cell death integrating pyroptosis, apoptosis, and necroptosis, has been implicated in cardiac injury and may represent a convergent mechanism linking inflammation and myocardial remodeling, but remains uninvestigated in HCM. - Source: PubMed
Publication date: 2026/01/07
Zhong JinlongZhao QinghuiWu RuiqingZhang ShuguangLiu GuoyiZhang ZhihuiHan XiaShi Lin - Inflammation-driven fibrosis represents a common pathological endpoint in both heart failure (HF) and chronic kidney disease (CKD), which together affect over 1 billion people worldwide. Understanding the shared molecular mechanisms by which inflammation contributes to the pathogenesis of HF and CKD is crucial for enabling early diagnosis and guiding the development of broad-spectrum therapeutic strategies. - Source: PubMed
Publication date: 2026/02/05
Hua LeiShen LiangruTao YongshouWang ChentongShao Xiaohang - Ischemia-reperfusion injury remains a major challenge in modern regenerative medicine due to its complex mechanisms, lack of effective therapies, and persistent constrains to translating new interventions from bench to bedside. Currently, there are no FDA-approved drugs that directly target ischemia-reperfusion injury, highlighting a substantial therapeutic gap. While restoring blood flow is vital for salvaging ischemic tissue, the reperfusion process paradoxically triggers additional cellular damage. The clinical significance and complexity of ischemia-reperfusion injury underscore an urgent need for mechanistically targeted therapeutic approaches. Recent research has identified pivotal molecular targets-PHLDA1, SIRT6, PKM2, and ubiquitin-specific proteases (USPs)-that play key roles in modulating cellular responses such as oxidative stress, inflammation, metabolism, apoptosis, autophagy, ferroptosis, and blood-brain barrier dysfunction during ischemia reperfusion injury. Advances in understanding these mechanisms offer promising strategies for developing novel interventions to mitigate tissue damage and improve patient outcomes. This review critically examines these molecular targets, detailing recent advances and outlining future directions in ischemia reperfusion injury research. - Source: PubMed
Bhujbal ShreeyaBhatt Lokesh Kumar