ADFP
- Known as:
- ADFP
- Catalog number:
- 001207A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADFP
Related genes to: ADFP
- Gene:
- PLIN2 NIH gene
- Name:
- perilipin 2
- Previous symbol:
- ADFP
- Synonyms:
- ADRP
- Chromosome:
- 9p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-07
- Date modifiied:
- 2014-11-18
Related products to: ADFP
Related articles to: ADFP
- Glioblastoma (GBM) remains a therapeutic challenge due to its resistance to standard chemotherapy and high recurrence rate. This study investigates the combined effects of alantolactone (ALT) and temozolomide (TMZ) on GBM cells, focusing on stemness, lipid metabolism, and the underlying Hippo signaling pathway. Human GBM cell lines U87 and U251 were treated with ALT and TMZ, either alone or in combination. Cell viability was assessed using the CCK-8 assay, stemness was evaluated by sphere formation assay, and gene and protein expression were analyzed by qPCR and Western blotting. A xenograft mouse model was established to evaluate in vivo efficacy. Phospho-kinase arrays and rescue experiments using the Hippo pathway inhibitor XMU-MP-1 were performed to explore the underlying mechanisms. The results showed that both ALT and TMZ inhibited cell proliferation in a dose-dependent manner. The combination treatment synergistically reduced cell viability, sphere formation, and the expression of stemness markers (CD133, NANOG, SOX2) and lipid metabolism regulators (PLIN2, FASN, SREBP1). In vivo, combined therapy significantly suppressed tumor growth and improved histopathological features. Mechanistically, ALT and TMZ promoted YAP1 phosphorylation and downregulated TEAD2, AXL, and c-MYC. Inhibition of Hippo signaling with XMU-MP-1 reversed the anti-tumor effects of the combination treatment. In conclusion, ALT and TMZ synergistically inhibit GBM growth and stemness by activating the Hippo pathway and suppressing lipid metabolism. These findings provide a rationale for the combined use of ALT and TMZ as a potential therapeutic strategy against GBM. - Source: PubMed
Publication date: 2026/05/13
Ren TongLi YishiZhou ChuanguangJiao YongqingGuo TianlinLi ZhiHu ChunyanZhao JunfengWang Xun - Systemic PPARγ agonist therapies have been investigated for clinical use in MASLD. Previous studies, however, have shown that PPARγ activation in hepatocytes worsens MASLD. Overall, the precise molecular mechanisms regulated by PPARγ in hepatocyte during MASLD remain incompletely defined. Hepatocyte-specific PPARγ knockout mice were fed a clinically-relevant fast-food diet (FFD) for 2 or 5-months to characterize the role of PPARγ in MASLD progression. PPARγ expression and activity were increased in murine FFD-model and in hepatocytes of human MASLD/MASH patients, based on single-nucleus RNA-sequencing analysis. PPARγ-deletion conferred protection against diet-induced steatosis, fibrosis, and liver injury by suppressing lipogenic, inflammatory, and fibrogenic signaling. Although de-novo fatty-acid synthesis was only modestly affected and compensated with disease progression, enhancement of lipolysis and suppression of lipid droplet stabilization machinery was persistent. PPARγ-deletion robustly inhibited expression and signaling-activity of TGFβ1, a master regulator of hepatic fibrosis, throughout the progression of MASLD. Importantly, a novel PPARγ-HNF4α regulatory axis in MASLD was identified, with increased HNF4α mRNA/protein expression and activation of its downstream metabolic networks in PPARγ-deficient livers. Further, integration of ChIP-seq and transcriptomic analysis revealed that HNF4α might be co-regulating a major fraction (>70%) of genes under direct control of PPARγ during MASLD. This study provides a comprehensive temporal framework for hepatocyte PPARγ function in MASLD, revealing an antagonistic PPARγ-HNF4α transcriptional network that governs hepatic metabolic fate. - Source: PubMed
Publication date: 2026/05/11
Bano ShehnazCopeland Matthew ALiu Jia-JunOrr AnneStoops John WMars Wendy MLiu SilviaLocker JosephMichalopoulos George KBhushan Bharat - Acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) remains the leading cause of treatment failure in advanced non-small cell lung cancer (NSCLC) patients harboring sensitizing EGFR mutations. This study aims to investigate the underlying resistance mechanisms in EGFR-mutated NSCLC. - Source: PubMed
Publication date: 2026/05/09
Shen JieGou LanyingSun YujieLuo PengHong ShuoZhang ChunyanSun YueqinShen WeitaoFang JianboZhang YuemingLi XuechunYing HaoxuanLyu QiongZhang JianWei Ting - Uterine leiomyomas may arise from somatic stem or progenitor cells, leading to abnormal activation, proliferation, and clonal expansion. In organ cultures of myometrium and leiomyoma, differentiated cells decline after 7 days, whereas resident stem cells may persist within their niches and subsequently become activated, proliferate, and repopulate tissue slices. This study investigated gene expression programs that regulate the proliferation and differentiation of myometrial and -mutant leiomyoma stem cells during long-term organ culture. - Source: PubMed
Publication date: 2026/04/22
Vázquez PaulaSalas AnaBeltrán-Flores SilviaMontes de Oca FranciscoDelgado AraceliAlmeida Teresa A - Astrocytes coordinate neuronal signaling in physiological conditions but can also drive neuroinflammation in pathophysiologic conditions, such as chronic pain. How and when astrocyte molecular pathways change in response to pain-inducing peripheral injury is key to understanding the acute-to-chronic pain transition. Here, we utilize translating ribosome affinity purification technology in a mouse model of complex regional pain syndrome to uncover the functional molecular signature of spinal astrocytes early and late post-injury. We find that astrocytes exhibit a temporally distinct translatome with most significant gene expression changes occurring acutely after injury. We further identify astrocyte lipid metabolism as altered after injury and demonstrate that lipid droplets (marked by PLIN2) accumulate in the spinal dorsal horn in the chronic post-injury phase. Overall, this work provides an astrocyte-specific translatome resource for understanding spinal astrocyte contributions to pain and highlights spinal cord lipid metabolism as a pathway of interest in pain pathophysiology. - Source: PubMed
Publication date: 2026/04/12
Siliezar-Doyle JanellePerez Richard KStauffenberg EmmaNippert Amy RTawfik Vivianne L