Insig2 antibody (FITC)
- Known as:
- Insig2 (anti-) (fluorecein)
- Catalog number:
- orb102835
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- Insig2 antibody (FITC)
Related genes to: Insig2 antibody (FITC)
- Gene:
- INSIG2 NIH gene
- Name:
- insulin induced gene 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q14.1-q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-17
- Date modifiied:
- 2018-02-13
Related products to: Insig2 antibody (FITC)
Related articles to: Insig2 antibody (FITC)
- Cystic echinococcosis, caused by the larval stage of Echinococcus granulosus, predominantly affects the liver. Components of hydatid cyst fluid (HCF), including extracellular vesicles (EVs), have been suggested to participate in host-parasite communication. The present study investigated whether HCF and EVs derived from it can influence insulin-related genes in hepatocyte cells. EVs were isolated from the HCF obtained from the liver of an infected sheep using differential centrifugation and were characterized by western blotting, scanning electron microscopy (SEM), dynamic light scattering (DLS), and zeta potential analysis. HepG2 cells were treated with EVs and HCF for 24 and 48 h. The expression of insulin-related genes, including INSR, AKT, IDE, and INSIG2, was then evaluated by quantitative real-time PCR. EV significantly up-regulated AKT (1.98 ± 0.17, p < 0.0001), INSR (2.09 ± 0.34, P = 0.0008), IDE (1.40 ± 0.17, P = 0.0031), and INSIG2 (1.67 ± 0.17, P = 0.0005) at 24 h; however, at 48 h, AKT (-2.68 ± 0.4), INSR (-3.75 ± 0.4), and IDE (-3.6 ± 0.93) were significantly down-regulated (all P < 0.0001), while INSIG2 remained up-regulated (3.81 ± 0.85, P = 0.0006). In contrast, HCF exposure predominantly caused gene down-regulation, with significant decreases in AKT (-1.41 ± 0.4), INSR (-1.9 ± 0.72), and IDE (-1.6 ± 0.34) at 24 h (all P ≤ 0.0002) and a more pronounced downregulation of all genes at 48 h, including AKT (-6.67 ± 1.56), INSR (-5.89 ± 0.76), IDE (-6.8 ± 1.2), and INSIG2 (-1.16 ± 0.06) (all P < 0.0001). Our findings showed that exposure to EVs was associated with reduced expression of INSR and AKT and increased expression of IDE and INSIG2. This metabolic reprogramming appears to be a coordinated strategy to divert host energetic resources to favor parasite survival. - Source: PubMed
Publication date: 2026/08/10
Zanjirani Farahani LeyliRouhani SoheilaNiyyati MaryamEslami NasimFasihi Harandi MajidMirjalali Hamed - Environmental exposure to persistent and non-persistent endocrine-disrupting chemicals (EDCs), including per- and polyfluoroalkyl substances (PFAS), polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), polycyclic aromatic hydrocarbons (PAHs), dioxins, phthalates, and bisphenols, has been increasingly associated with elevated cardiovascular disease (CVD) risk. Emerging evidence suggests the importance of gene-environment interactions in modulating individual susceptibility to EDC-related cardiovascular effects. This review summarizes current knowledge by synthesizing the main classes of EDCs, evaluating the evidence linking them to cardiovascular outcomes, and highlighting how genetic variability may modulate EDC-induced cardiovascular risk. Across the studies analyzed, the most extensively investigated genetic polymorphisms involve pathways related to oxidative stress regulation, xenobiotic metabolism and detoxification, hormone signaling, and lipid homeostasis. Variants in antioxidant defense genes, such as , , and , have been associated with increased hypertension risk and vascular dysfunction following exposure to bisphenols and PAHs. Polymorphisms in , , CYP1A2, CYP2E1, , and may influence susceptibility to cardiometabolic alterations and congenital heart defects, whereas variants in , , , and have been linked to obesity, dyslipidemia, and hypertension associated with PFAS, PBDEs, and bisphenols. A deeper understanding of gene-environment interactions is essential to advance preventive cardiology and mitigate the cardiovascular impact of environmental pollutants. - Source: PubMed
Publication date: 2026/06/21
Palazzo MariangelaGorini FrancescaSimonini LudovicaMinichilli FabrizioBorghini Andrea - Alternative polyadenylation (APA) is a key post-transcriptional regulatory mechanism in eukaryotes, but its role in adipogenesis remains poorly understood. Here, we investigated how insulin-induced gene 2 (Insig2) APA regulates adipogenesis. Functional assays showed that Insig2 knockdown promoted 3T3-L1 preadipocyte differentiation, whereas Insig2 overexpression inhibited it. During adipogenesis, Insig2 generated two APA isoforms with distinct 3'UTR lengths, and the short 3'UTR isoform was more abundant than the long isoform. Mechanistically, miR-96-5p specifically targeted the unique extension region of the long Insig2 3'UTR isoform to suppress its expression, thereby alleviating its inhibitory effect on adipogenesis. In contrast, the short Insig2 isoform lacked the miR-96-5p binding site and escaped miR-96-5p-mediated repression, thus exerting a stronger inhibitory effect on adipogenesis. Collectively, these findings reveal an isoform-specific Insig2 APA/miR-96-5p regulatory axis that dynamically controls adipogenesis at the post-transcriptional level. Our results revealed a new regulatory mechanism of Insig2 APA in adipogenesis. - Source: PubMed
Publication date: 2026/06/23
Ren ShizhongQin XuyongZhang LichunLi ChengpingYu YuanyuanZhou WenhaoZhao MeimanZhou Guoli - The sterol response element binding proteins (SREBPs), SREBP-1a/c and SREBP-2, are sterol-regulated transcription factors that control the expression of cholesterol and fatty acid-raising genes. Elevated expression of SREBPs has been linked to increased morbidity and mortality rates associated with conditions including obesity, cancer, and cardiovascular disease. Therefore, the development of new therapeutics to inhibit SREBP activity may be beneficial for treating various diseases associated with altered lipid levels. In their inactive state, SREBPs remain sequestered in the ER membrane in a complex with SREBP cleavage activating protein (SCAP) and one of two ER-anchoring proteins, Insig-1 or Insig-2. Activation proceeds through dissociation of SREBP/SCAP from Insigs, SCAP-assisted translocation to the Golgi, proteolytic membrane release and nuclear import. We employed a high-throughput enzyme complementation assay to identify inhibitors of SREBP-2 translocation to the nucleus, resulting in the identification of VB-84922 having an IC value of 0.45 ± 0.052 μM. VB-84922-mediated inhibition of nuclear translocation was confirmed by fluorescence microscopy with an mNeonGreen-SREBP-2 fusion protein. Crucially, VB-84922 inhibited the lovastatin-induced activity of an SREBP-responsive reporter construct and suppressed the expression of endogenous SREBP target genes. Co-transfection assays using an SREBP reporter and fluorescence microscopy were used to delineate the target of VB-84922 in the SREBP activation pathway. The drug blocked ER export of wild-type SCAP but had no effect on SREBP activity in cells expressing the nuclear form of SREBP-1a, or mutated versions of SCAP that are unable to bind Insigs and that chaperone SREBP to the Golgi constitutively. These results suggest that VB-84922 targets a step upstream of ER export in the SREBP activation cascade. VB-87496, a therapeutic lead compound, developed from VB-84922, demonstrated efficacy within a murine acute fasting-refeeding model by inhibiting full-length SREBP protein maturation and SREBP-dependent transcription. VB-87496 represents a specific SREBPs-SCAP inhibitor that has potential for further lead optimization medicinal chemistry efforts to generate a potent and selective pre-clinical candidate for treating lipid-related diseases. - Source: PubMed
Publication date: 2026/03/24
Corbalan J JoseSchormann WiebkeJagadeesan PranaviKale JustinHuang Yu-ChiangSiegel RachaelBeasley James RTung Jyun-PengNohturfft AxelAndrews DavidNickels Joseph T - Metabolic dysfunction-associated steatotic liver disease (MASLD) ranges from simple steatosis (MASL) to fibrotic steatohepatitis (MASH). Yet, the molecular mechanisms initiating these divergent outcomes remain unclear. We addressed the question whether MASLD induced by a high-sucrose/starch diet (MCS) is similar to a high-fat, methionine- and choline-deficient diet (MCD+HFD). To investigate early genomic programming events in these MASLD models, we fed C57BL/6N mice either an MCS or MCD+HFD for 14 days. Histopathology and serum biochemistries confirmed MASLD phenotypes and transcriptomics guided pathway enrichment analysis. Furthermore, ChIP-seq-validated transcription factor targets enabled construction of regulatory gene networks (RGNs) in glucose homeostasis and lipid metabolism. Importantly, the MCS and MCD+HFD caused 692 and 703 differentially expressed genes, and although transcriptomics revealed shared genomic responses, we also observed diet-specific adaptations. Both diets repressed glycolysis, yet MCS showed broader suppression. Furthermore, fatty acid β-oxidation and lipid droplet biogenesis was induced whereas lipogenesis, cholesterol biosynthesis and the kynurenine pathway were repressed. Strikingly, the high-sucrose/high-starch diet suppressed acute-phase, prostaglandin, redox, antigen presentation, and autophagy pathways. Conversely, the high-fat MCD-diet activated cytokine signaling, macrophage networks, and inflammatory programs. Intriguingly, RGNs aided an identification of diet-specific master regulatory networks with MCS stimulating Insig2, Id1, and Mafb signaling. Conversely, the high-fat MCD-diet silenced Srebf1, Scd1, and Acly. Together, our findings highlight early genomic reprogramming events in MASLD, and unlike the high-fat MCD-diet which stimulates MASH, we report high-sucrose/high-starch to elicit benign steatosis without inflammation. - Source: PubMed
Publication date: 2026/03/20
Xu YanzheZhu YunLee KyuhongBorlak Jürgen