PHAS_I pAb;human, mouse, rat
- Known as:
- PHAS_I pAb;H. sapiens, mouse, rat
- Catalog number:
- ASAKAP-MA110C
- Product Quantity:
- 25 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- PHAS_I pAb;human mouse rat
Related products to: PHAS_I pAb;human, mouse, rat
Related articles to: PHAS_I pAb;human, mouse, rat
- The study aimed to evaluate the effects of full-fat rice bran (FFRB; Tainung No. 81, Taiwan) at various doses on insulin resistance, muscle atrophy, and gut microbiota composition in middle-aged ovariectomized (OVX) mice fed a high-fat diet (HFD), using young sham-operated mice as a life-stage reference group. Thirty-six female ICR mice were assigned to six groups, including OVX mice fed HFD with or without 5%, 10%, or 20% FFRB. Compared with HFD-fed OVX controls, 20% FFRB reduced body weight gain by 43%, decreased visceral fat mass, and improved insulin resistance (homeostasis model assessment of insulin resistance, HOMA-IR reduced by 65%, = 0.001). FFRB attenuated the decline in relative grip strength (forelimb, = 0.013; four-limb, < 0.001), and upregulated muscle protein synthesis genes, including insulin receptor substrate 1 (IRS-1), mammalian target of rapamycin (mTOR), eukaryotic translation initiation factor 4E binding protein 1 (eIF-4EBP1), while downregulating forkhead box protein O1 (FOXO1), muscle RING-finger protein-1 (MuRF-1), and interleukin (IL)-6. FFRB was also associated with higher fecal acetate levels ( < 0.001), upregulated colonic tight junction genes (occludin and zonula occludens (ZO)-1), and greater relative abundance of . Correlation analyses revealed positive associations between short-chain fatty acids (SCFAs) and muscle strength, muscle anabolic markers, genus , and . Dietary inclusion of FFRB was associated with favorable metabolic and muscle-related parameters in HFD-fed middle-aged OVX mice, with potential involvement of gut microbiota and SCFA alterations. - Source: PubMed
Publication date: 2026/05/30
Loe Pei YuOhsaki YusukeYang Suh-ChingShirakawa HitoshiChiu Wan-Chun - Early liver metastasis is a major factor contributing to the poor prognosis of pancreatic ductal adenocarcinoma (PDAC). Single-cell RNA sequencing (scRNA-seq) can analyze the heterogeneity between the primary tumor and metastatic lesions, but its wide clinical application is limited by costs, tissue requirements, and analytical complexity. In contrast, H&E-stained sections are more commonly available. However, it is not clear whether the risk signals derived from images can truly reflect the biological characteristics related to metastasis. We integrated the single-cell RNA sequencing data (GSE154778) of primary and metastatic pancreatic ductal adenocarcinoma (PDAC) with TCGA transcriptome, clinical pathological, and H&E image data. The copy number pattern based on InferCNV was used to distinguish malignant ductal cells with high copy numbers from ductal cells with low copy numbers. Differential expression and LASSO screening identified a transfer-related feature consisting of four genes (ARHGAP18, ASPH, EIF4EBP1, LY6D), and this feature was subsequently associated with image-derived features extracted through a dual-stream pathomics pipeline. The reproducibility of transcriptional levels in prognosis was evaluated in six independent GEO PDAC subgroups, and the locked pathological model was further tested on an external CPTAC subset using frozen cutoff values from TCGA. Pseudotime analysis suggested that a subset of metastatic malignant ductal cells occupied a progenitor-like transcriptional state. Cell-cell communication analysis indicated reduced antigen-presentation/prostaglandin-related signaling and relative enrichment of MIF- and laminin-associated pathways in metastases. The pathology model retained prognostic stratification in the internal TCGA validation split, although discrimination was lower than in training. Across six external GEO cohorts analyzed with cohort-specific optimal cutoffs, LY6D showed significant adverse survival associations in four cohorts, ARHGAP18 and ASPH in three cohorts each, and EIF4EBP1 in one cohort. In the external CPTAC cohort, the locked pathomics score also remained prognostic (HR 1.60, 95% CI 1.11-2.30; log-rank P = 0.011), with 12-, 24-, and 36-month time-dependent AUCs of 0.635, 0.617, and 0.639. This study presents an integrative genotype-to-phenotype workflow linking scRNA-seq-derived metastatic features to routine pathology images. External transcript-level validation and supportive CPTAC pathomics evaluation strengthen the findings, but larger independent validation studies and mechanistic experiments remain necessary before any clinical translation. - Source: PubMed
Publication date: 2026/05/26
Bao WenhaoLeng KaimingXia XiaodanChang JingyuYing PengchaoLuan ShaohaiYuan Qihua - Hippocampal neural stem cells (NSCs) proliferation and differentiation are crucial for neuroregeneration, but their regulation remains unclear. This study investigates the role of the RNA methyltransferase Mettl8 in NSCs' fate determination. - Source: PubMed
Xu JiaminXu LipingLi YangKong XuejianMa WenhuiXie LinjieLyu YingXuan Aiguo - Metabolic dysfunction-associated steatohepatitis (MASH) is emerging as a leading cause of chronic liver disease. MTOR (mechanistic target of rapamycin kinase) complex 1 (MTORC1) is a potential therapeutic target, whereas suppression of total MTORC1 activity can lead to unwanted effects. Here, we found that byakangelicin (Bya), a natural compound, selectively inhibited MTORC1-mediated phosphorylation of TFEB (transcription factor EB), without affecting canonical MTORC1 substrates. Knockout of hepatic blocked the alleviation effects of Bya on hepatic steatosis, inflammation, insulin resistance, and fibrosis in mice, while reintroduction of TFEB restored these effects. We identified Bya directly bound to MET370 and PHE552 of FLCN (folliculin), suppressing the function of the FLCN-FNIP1 (folliculin interacting protein 1)/FNIP2 complex, which in turn inhibited MTORC1-mediated cytoplasmic sequestration of TFEB. Mutation of FLCN (M370A and F552A) in the liver abolished Bya-induced protection against MASH. Thus, Bya is a promising therapeutic natural compound for MASH, and selective inhibition of MTORC1 is a potential approach to treat this disease. aa, amino acids; AAV, adeno-associated virus; Bio, biotin; Bio-Bya, biotin-conjugated Bya; BSA, bovine serum albumin; BW, body weight; Bya, byakangelicin; CETSA, cellular thermal shift assay; CHIP-atlas, chromatin immunoprecipitation atlas; C, maximum concentration; CQ, chloroquine; DARTS; drug affinity responsive target stability assay; EIF4EBP1/4E-BP1, eukaryotic translation initiation factor 4E binding protein 1; FBS, fetal bovine serum; FDA, food and drug administration; FIMO-JASPAR, find individual motif occurrences-JASPAR; FLCN, folliculin; FNIP1, folliculin interacting protein 1; GAP, GTPase-activating protein; GOT1/AST, glutamic-oxaloacetic transaminase 1; GPT/ALT, glutamic-pyruvic transaminase; GTRD, gene transcription regulatory database; GTT, glucose tolerance test; H&E, hematoxylin and eosin; Hbonds, hydrogen bonds; HFD, high-fat diet; HFHC, high-fat and high-cholesterol; HOMA-IR, homeostatic model assessment of insulin resistance; HSCs, hepatic stellate cells; IP, immunoprecipitation; ITT, insulin tolerance test; K, dissociation constant; KEGG, kyoto encyclopedia of genes and genomes; KPBS, potassium phosphate-buffered saline; LC-MS/MS, liquid chromatography-tandem mass spectrometry; LW/BW, liver-to-body weight ratio; MAP1LC3/LC3, microtubule associated protein 1 light chain 3; MASH, metabolic dysfunction-associated steatohepatitis; MASLD, metabolic dysfunction-associated steatotic liver disease; MCD, methionine and choline deficient; MST, microscale thermophoresis assay; MTOR, mechanistic target of rapamycin kinase; MTORC1, MTOR complex 1; ND, normal diet; NFKB/NF-κB, nuclear factor kappa B; NFKBIA/IKBA, NFKB inhibitor alpha; OP, oleate acid and palmitate acid; PBS, phosphate-buffered saline; PCA, principal component analysis; qRT-PCR, real-time quantitative PCR; RELA/p65, RELA proto-oncogene, NF-kB subunit; Res, resmetirom; Rg, radius of gyration; RMSD, root-mean-square deviation; RMSF, root-mean-square fluctuation; RPS3, ribosomal protein S3; RPS6KB1/S6K1, ribosomal protein S6 kinase B1; RRAGC, ras related GTP binding C; SASA, solvent-accessible surface area; SNRPD2, small nuclear ribonucleoprotein D2 polypeptide; SQSTM1/p62, sequestosome 1; T, half-life; TFE3, transcription factor binding to IGHM enhancer 3; TFEB, transcription factor EB; TMEM192, transmembrane protein 192; VIM, vimentin; WT, wild-type. - Source: PubMed
Publication date: 2026/05/25
Du XiliangFang ZhiyuanLiu GuowenWang LiJu LingxueGao WenwenSong YuxiangLei LinLi Xinwei - The ability to adapt to nutrient stress, such as amino acid limitation, is crucial for cell survival. The mTORC1 complex and integrated stress response (ISR) are two mechanisms that sense the availability of amino acids and regulate protein synthesis. Here, we reveal a new SIRT2-mediated pathway, downstream of the ISR, that is activated under amino acids limitation to suppress global translation. Under amino acid deprivation, SIRT2 protein level is upregulated translationally by its upstream open reading frame (uORF). SIRT2 in turn suppresses translation, which helps cells to survive amino acid limitation. We identify eukaryotic translation initiation factor 4E (eIF4E) binding protein 1 (4E-BP1), which binds to eIF4E and inhibits translation, as a substrate of SIRT2. SIRT2 deacetylates 4E-BP1 at lysine 69 and stabilizes 4E-BP1 by protecting it from proteasomal degradation, leading to suppression of global translation. Our study uncovers a role for SIRT2 in regulating translation and identifies a new regulatory mechanism of 4E-BP1 in cells. - Source: PubMed
Publication date: 2026/05/18
Zi YanlinZhao JiaqiWang MiaoHou DanCerione Richard ALin Hening