bHLHd1,BHLHD1,Class D basic helix-loop-helix protein 1,Homo sapiens,Human,SREBF1,SREBP1,SREBP-1,Sterol regulatory element-binding protein 1,Sterol regulatory element-binding transcription factor 1
- Known as:
- bHLHd1,BHLHD1,Class D basic helix-loop-helix protein 1,Homo sapiens,Human,SREBF1,SREBP1,SREBP-1,Sterol regulatory element-binding protein 1,Sterol regulatory element-binding transcription factor 1
- Catalog number:
- EIAAB39838
- Category:
- -
- Supplier:
- EIAab
- Gene target:
- bHLHd1 BHLHD1 Class basic helix-loop-helix protein 1 Homo sapiens Human SREBF1 SREBP1 SREBP-1 Sterol regulatory element-binding transcription factor
Related genes to: bHLHd1,BHLHD1,Class D basic helix-loop-helix protein 1,Homo sapiens,Human,SREBF1,SREBP1,SREBP-1,Sterol regulatory element-binding protein 1,Sterol regulatory element-binding transcription factor 1
- Gene:
- MLX NIH gene
- Name:
- MAX dimerization protein MLX
- Previous symbol:
- TCFL4
- Synonyms:
- MAD7, MXD7, bHLHd13
- Chromosome:
- 17q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-10
- Date modifiied:
- 2019-01-21
- Gene:
- MLXIPL NIH gene
- Name:
- MLX interacting protein like
- Previous symbol:
- WBSCR14
- Synonyms:
- WS-bHLH, MIO, CHREBP, MONDOB, bHLHd14
- Chromosome:
- 7q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-20
- Date modifiied:
- 2016-03-14
- Gene:
- SREBF1 NIH gene
- Name:
- sterol regulatory element binding transcription factor 1
- Previous symbol:
- -
- Synonyms:
- SREBP1, bHLHd1, SREBP-1c, SREBP1a
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-23
- Date modifiied:
- 2016-02-03
Related products to: bHLHd1,BHLHD1,Class D basic helix-loop-helix protein 1,Homo sapiens,Human,SREBF1,SREBP1,SREBP-1,Sterol regulatory element-binding protein 1,Sterol regulatory element-binding transcription factor 1
Related articles to: bHLHd1,BHLHD1,Class D basic helix-loop-helix protein 1,Homo sapiens,Human,SREBF1,SREBP1,SREBP-1,Sterol regulatory element-binding protein 1,Sterol regulatory element-binding transcription factor 1
- Hepatic steatosis signifies onset of metabolic dysfunction-associated fatty liver disease (MAFLD) caused by disrupted metabolic homeostasis compromising liver function. Regular consumption of common beans reduces the risk of metabolic impairment, but its effective dose, the impact of biological sex, and underlying mechanisms of action are unknown. We fed female and male C57BL6/J mice with obesogenic yet isocaloric diets containing 0%, 17.5%, 35%, and 70% of total dietary protein derived from cooked whole common beans. Liver tissue was collected for histopathology, lipid quantification, and RNA-seq analyses. Beans qualitatively and quantitatively diminished hepatic fat deposition at the 35% dose in female and 70% dose in male mice. Bean-induced differentially expressed genes (DEGs) most significantly mapped to hepatic steatosis and revealed dose-responsive inhibition of lipogenesis markers (, , , , , etc.) and triacylglycerol biosynthesis, activation of triacylglycerol degradation, and downregulation of sterol regulatory element-binding transcription factor 1 (SREBF1) signaling. Upregulated fatty acid β-oxidation was more prominent in females, while suppression of -mediated fatty acid uptake-in males. Sex-dependent bean effects also involved DEGs patterns downstream of peroxisome proliferator-activated receptor α (PPARα) and MLX-interacting protein-like (MLXIPL). Therefore, biological sex determines amount of common bean in the diet required to prevent hepatic lipid accumulation. - Source: PubMed
Publication date: 2023/01/19
Lutsiv TymofiyMcGinley John NNeil Elizabeth SFoster Michelle TThompson Henry J - Autophagic pathways cross with lipid homeostasis and thus provide energy and essential building blocks that are indispensable for liver functions. Energy deficiencies are compensated by breaking down lipid droplets (LDs), intracellular organelles that store neutral lipids, in part by a selective type of autophagy, referred to as lipophagy. The process of lipophagy does not appear to be properly regulated in fatty liver diseases (FLDs), an important risk factor for the development of hepatocellular carcinomas (HCC). Here we provide an overview on our current knowledge of the biogenesis and functions of LDs, and the mechanisms underlying their lysosomal turnover by autophagic processes. This review also focuses on nonalcoholic steatohepatitis (NASH), a specific type of FLD characterized by steatosis, chronic inflammation and cell death. Particular attention is paid to the role of macroautophagy and macrolipophagy in relation to the parenchymal and non-parenchymal cells of the liver in NASH, as this disease has been associated with inappropriate lipophagy in various cell types of the liver.: ACAT: acetyl-CoA acetyltransferase; ACAC/ACC: acetyl-CoA carboxylase; AKT: AKT serine/threonine kinase; ATG: autophagy related; AUP1: AUP1 lipid droplet regulating VLDL assembly factor; BECN1/Vps30/Atg6: beclin 1; BSCL2/seipin: BSCL2 lipid droplet biogenesis associated, seipin; CMA: chaperone-mediated autophagy; CREB1/CREB: cAMP responsive element binding protein 1; CXCR3: C-X-C motif chemokine receptor 3; DAGs: diacylglycerols; DAMPs: danger/damage-associated molecular patterns; DEN: diethylnitrosamine; DGAT: diacylglycerol O-acyltransferase; DNL: lipogenesis; EHBP1/NACSIN (EH domain binding protein 1); EHD2/PAST2: EH domain containing 2; CoA: coenzyme A; CCL/chemokines: chemokine ligands; CCl carbon tetrachloride; ER: endoplasmic reticulum; ESCRT: endosomal sorting complexes required for transport; FA: fatty acid; FFAs: free fatty acids; FFC: high saturated fats, fructose and cholesterol; FGF21: fibroblast growth factor 21; FITM/FIT: fat storage inducing transmembrane protein; FLD: fatty liver diseases; FOXO: forkhead box O; GABARAP: GABA type A receptor-associated protein; GPAT: glycerol-3-phosphate acyltransferase; HCC: hepatocellular carcinoma; HDAC6: histone deacetylase 6; HECT: homologous to E6-AP C-terminus; HFCD: high fat, choline deficient; HFD: high-fat diet; HSCs: hepatic stellate cells; HSPA8/HSC70: heat shock protein family A (Hsp70) member 8; ITCH/AIP4: itchy E3 ubiquitin protein ligase; KCs: Kupffer cells; LAMP2A: lysosomal associated membrane protein 2A; LDs: lipid droplets; LDL: low density lipoprotein; LEP/OB: leptin; LEPR/OBR: leptin receptor; LIPA/LAL: lipase A, lysosomal acid type; LIPE/HSL: lipase E, hormone sensitive type; LIR: LC3-interacting region; LPS: lipopolysaccharide; LSECs: liver sinusoidal endothelial cells; MAGs: monoacylglycerols; MAPK: mitogen-activated protein kinase; MAP3K5/ASK1: mitogen-activated protein kinase kinase kinase 5; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MCD: methionine-choline deficient; MGLL/MGL: monoglyceride lipase; MLXIPL/ChREBP: MLX interacting protein like; MTORC1: mechanistic target of rapamycin kinase complex 1; NAFLD: nonalcoholic fatty liver disease; NAS: NAFLD activity score; NASH: nonalcoholic steatohepatitis; NPC: NPC intracellular cholesterol transporter; NR1H3/LXRα: nuclear receptor subfamily 1 group H member 3; NR1H4/FXR: nuclear receptor subfamily 1 group H member 4; PDGF: platelet derived growth factor; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PLIN: perilipin; PNPLA: patatin like phospholipase domain containing; PNPLA2/ATGL: patatin like phospholipase domain containing 2; PNPLA3/adiponutrin: patatin like phospholipase domain containing 3; PPAR: peroxisome proliferator activated receptor; PPARA/PPARα: peroxisome proliferator activated receptor alpha; PPARD/PPARδ: peroxisome proliferator activated receptor delta; PPARG/PPARγ: peroxisome proliferator activated receptor gamma; PPARGC1A/PGC1α: PPARG coactivator 1 alpha; PRKAA/AMPK: protein kinase AMP-activated catalytic subunit; PtdIns3K: class III phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; PTEN: phosphatase and tensin homolog; ROS: reactive oxygen species; SE: sterol esters; SIRT1: sirtuin 1; SPART/SPG20: spartin; SQSTM1/p62: sequestosome 1; SREBF1/SREBP1c: sterol regulatory element binding transcription factor 1; TAGs: triacylglycerols; TFE3: transcription factor binding to IGHM enhancer 3; TFEB: transcription factor EB; TGFB1/TGFβ: transforming growth factor beta 1; Ub: ubiquitin; UBE2G2/UBC7: ubiquitin conjugating enzyme E2 G2; ULK1/Atg1: unc-51 like autophagy activating kinase 1; USF1: upstream transcription factor 1; VLDL: very-low density lipoprotein; VPS: vacuolar protein sorting; WIPI: WD-repeat domain, phosphoinositide interacting; WDR: WD repeat domain. - Source: PubMed
Publication date: 2021/04/02
Filali-Mouncef YasminaHunter CatherineRoccio FedericaZagkou StavroulaDupont NicolasPrimard CharlotteProikas-Cezanne TassulaReggiori Fulvio - Previous genome-wide association studies (GWAS) in multiple populations identified several genetic loci for coronary heart diseases (CHD). Here we utilized a 2-stage candidate gene association strategy in Chinese Han population to shed light on the putative association between several metabolic-related candidate genes and CHD. At the 1(st) stage, 190 patients with CHD and 190 controls were genotyped through the MassARRAY platform. At the 2(nd) stage, a larger sample including 400 patients and 392 controls was genotyped by the High Resolution Melt (HRM) method to confirm or rule out the associations with CHD. MLXIP expression level was quantified by the real time PCR in 65 peripheral blood samples. From the 21 studied single nucleotide polymorphisms (SNPs) of seven candidate genes: MLXIPL, MLXIP, MLX, ADIPOR1, VDR, SREBF1 and NR1H3, only one tag SNP rs4758685 (T→C) was found to be statistically associated with CHD (P-value = 0.02, Odds ratio (OR) of 0.83). After adjustment for the age, sex, lipid levels and diabetes, the association remained significant (P-value = 0.03). After adjustment for the hypertension, P-value became 0.20 although there was a significant difference in the allele distribution between the CHD patients with hypertension and the controls (P-value = 0.04, 406 vs 582). In conclusion, among the 21 tested SNPs, we identified a novel association between rs4758685 of MLXIP gene and CHD. The C allele of common variant rs4758685 interacted with hypertension, and was found to be protective against CHD in both allelic and genotypic models in Chinese Han population. - Source: PubMed
Publication date: 2013/06/26
Alobeidy Barrak FLi CongAlzobair Alya ALiu TaoZhao JunzhangFang YuanZheng Fang - Adipocyte differentiation is probably controlled by transcriptional and post-transcriptional regulation. Longissimus lumborum from Angus steers (aged 155 d; seven animals per diet) fed high-starch or low-starch diets for 112 d (growing phase) followed by a common high-starch diet for an additional 112 d (finishing phase) was biopsied at 0, 56, 112 and 224 d for transcript profiling via quantitative PCR of twenty genes associated with adipogenesis and energy metabolism. At 56 d steers fed high starch had greater expression of PPARgamma as well as the lipogenic enzymes ATP citrate lyase (ACLY), glucose-6-phosphate dehydrogenase (G6PD), fatty acid synthase (FASN), fatty acid binding protein 4 (FABP4), stearoyl-CoA desaturase (SCD), glycerol-3-phosphate acyltransferase, mitochondrial (GPAM), and diacylglycerol O-acyltransferase homologue 2 (DGAT2), and the adipokine adiponectin (ADIPOQ). Expression of insulin-induced gene 1 (INSIG1) was also greater with high starch at 56 d. Steers fed low starch experienced a marked increase in FASN, FABP4, SCD, DGAT2 and thyroid hormone-responsive (SPOT14 homologue, rat) (THRSP) between 56 and 112 d of feeding. A greater expression of the transcription factors sterol regulatory element-binding transcription factor 1 (SREBF1) and MLX interacting protein-like (MLXIPL) was observed at 224 d in steers fed high starch, suggesting a nutritional imprinting effect. Carryover effects of low starch feeding were discerned by greater expression at 224 d of THRSP, FABP4, SCD and DGAT2. These steers also had greater PPARgamma at 224 d. Despite these responses, low starch led to greater expression at 224 d of nuclear receptor subfamily 2, group F, member 2 (NR2F2), a known repressor of rodent adipocyte differentiation through its negative effects on PPARgamma, ADIPOQ and FABP4. Results suggested that early exposure to high starch induced precocious intramuscular adipocyte proliferation and metabolic imprinting of lipogenic transcription regulators. Low starch might have blunted the PPARgamma-driven adipogenic response through up-regulation of NR2F2 but the endogenous ligand for this nuclear receptor remains unknown. - Source: PubMed
Publication date: 2009/12/21
Graugnard Daniel EBerger Larry LFaulkner Dan BLoor Juan J