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
- Macrophages play an indispensable role in the pathogenesis of aortic dissection (AD). However, the underlying molecular and cellular mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2026/08/28
Li ZhenghaoChen HaonanLiu XuanyuShao YuePeng YindingWu QingchenShi HaomingZhang Cheng - Liver transplantation is the standard treatment for end-stage liver disease, but donor organ shortage has increased the use of marginal donor livers (eg, steatotic grafts). These livers are highly sensitive to liver ischemia/reperfusion injury (LIRI), worsening transplant outcomes, with unclear molecular mechanisms limiting targeted therapies. - Source: PubMed
Publication date: 2026/09/03
Lu KaiZhao Yi-MingChai Kui-YuanLyu YiZhang Xu-Feng - Perfluorooctane sulfonate (PFOS), a persistent environmental pollutant, has been implicated in metabolic dysfunction-associated steatotic liver disease (MASLD), yet the underlying molecular mechanisms remain incompletely characterized. We constructed an integrated analytical framework combining population epidemiology, network toxicology, machine learning, transcriptomic analysis, single-cell mapping, molecular docking, and experimental validation. NHANES data (n = 1,834) were analyzed to assess the association between serum PFOS concentrations and FLI-defined MASLD. Machine-learning analyses using LASSO and SVM-RFE prioritized candidate genes from 874 overlapping PFOS-MASLD-associated genes. Single-cell RNA sequencing resolved cell-type-specific expression patterns, while molecular docking evaluated potential PFOS-protein interactions. A 12-week murine exposure model provided in vivo validation. Epidemiological analysis identified a nonlinear association between serum PFOS and MASLD odds (p < 0.001), with effects evident at background exposure levels (7.76 ng/mL). Convergent machine-learning analyses prioritized five candidate genes: CYP7A1, GRIA3, PHLDA1, SOCS2, and WNT5A. An exploratory five-gene model yielded an apparent AUC of 0.998 (95% CI 0.993-0.998) within the analyzed transcriptomic dataset. Single-cell analysis revealed cell-type specificity, with CYP7A1/PHLDA1 enriched in hepatocytes, SOCS2/WNT5A in hepatic stellate cells, and GRIA3 in T cells. Molecular docking predicted potential PFOS-protein interactions with the five candidate targets, with docking scores ranging from -6.3 to -9.3 kcal/mol. RT-qPCR analysis of PFOS-treated mouse liver showed transcriptional changes consistent with the computational predictions. PFOS-treated mice exhibited hepatic lipid accumulation, elevated liver injury markers, and lipid dysregulation. Together, these findings support an association between PFOS exposure and MASLD-related hepatic dysfunction and propose a hypothesis-generating immune-metabolic framework requiring prospective and direct mechanistic validation. - Source: PubMed
Publication date: 2026/09/05
Zuo XuleiTan ShiyiHou XiaoyuZhang CongZhang YuxiZhang Juan - The emphysematous phenotype is an important phenotype in chronic obstructive pulmonary disease (COPD), with substantial morbidity and mortality. The mechanisms underpinning the role of alveolar type II (AT2) cells in alveolar repair within this phenotype remain poorly understood. This study aimed to elucidate the role of PHLDA1, a potential stemness regulator in AT2 cells, on emphysema development. Utilizing mice model, we performed a targeted knockdown of PHLDA1 in AT2 cells and subsequently exposed these mice to tobacco smoke to assess the resultant severity of emphysema and related alveolar damage. We manipulated PHLDA1 expression in AT2 cells line or primary mouse AT2 cells to examine its influence on AT2 stemness-related processes- differentiation, proliferation, and wound closure ability. The specific pathway of PHLDA1 mediated in AT2 cells, as well as its interaction with the GLI1 protein, was further investigated. Mice with reduced PHLDA1 expression developed the emphysema independent of smoking exposure. PHLDA1 knockdown in AT2 cells attenuated their proliferation via the Hedgehog pathway, impairing wound closure ability in the emphysematous phenotype. We also discovered a binding relationship between PHLDA1 and GLI1, where PHLDA1 modulates the nuclear translocation of GLI1, thus regulating the Hedgehog pathway and influencing the stemness and proliferation of AT2 cells. Our study suggests that PHLDA1 is a critical factor in the proliferation process of AT2 cells via modulation of GLI1 nuclear translocation. This regulation is essential to the pathogenesis of the emphysematous phenotype in COPD, signifying potential therapeutic targets for intervention. - Source: PubMed
Publication date: 2026/07/04
Bai ShuangWang ShuaifuYe RuiWang DiMa MingxinZhao Li - Excessive lipid accumulation is a hallmark of metabolic disorders which includes obesity and insulin resistance; however, effective therapeutic strategies remain limited. Tamarixetin (Tx), a naturally occurring flavonoid with diverse pharmacological properties, has not been fully characterized in the context of lipid metabolism. In this study, we explored the metabolic benefits and molecular mechanisms of Tx in a Western diet (WD)-induced obesity model. Transcriptomic profiling revealed that Tx reversed WD-induced gene expression patterns, notably suppressing and inducing expression. Mechanistically, docking analysis suggested that Tx interacts with the acetyl-CoA-binding region within the p300 histone acetyltransferase domain, thereby attenuating H3K9 acetylation at the Pdk4 promoter. This epigenetic inhibition of led to activation of the p38/AMPK signaling cascade, upregulation of and , and enhanced insulin sensitivity . Collectively, our findings identify Tx as a novel epigenetic modulator that simultaneously suppresses lipogenic gene expression and restores metabolic signaling. Given its natural origin and multifaceted mode of action, Tx emerges as a promising candidate for therapeutic intervention in metabolic disorders. - Source: PubMed
Publication date: 2026/06/30
Song Ji-HyeLee JanghoKim Hyo-JinLee Jae-InLee Yu GeonChoi Hyo-KyoungHwang Jin-Taek