Browse our anti-INSIG1 (INSIG1) Antibodies

Human Insulin Induced Gene 1 (INSIG1) interaction partners

1. Knock down of FADS1 did not significantly change cholesterol efflux (p=0.70), but knockdown of INSIG1 and LDLR resulted in highly significant reduction of the efflux to HDL (67% and 75% of control, respectively, p<0.001).

2. INSIG1 variation may contribute to statin-induced changes in plasma triglycerides in a sex-specific manner.

3. argue that precursor miR-122 molecules modulate polyadenylation site usage in Insig1 mRNAs, resulting in down-regulation of Insig1 protein abundance

4. Our findings suggest that miR-92a may affect cholesterol metabolism by repressing insig1, resulting in raised intracellular cholesterol levels and Golgi volume and hence enhanced protein secretion.

5. identified interaction of three genes in INSIG-SCAP-SREBP pathway on risk of obesity, revealing that these genes affect obesity more likely through a complex interaction pattern than single gene effect.

6. Data show the essential role of PPARgamma and PPARgamma coactivator 1alpha (PGC-1alpha) in up-regulating Insig-1/2 expression, defining a mechanistic pathway triggered by CD36, and leading to cholesterol depletion in hepatocytes.

7. Our results indicated that the dysregulation of INSIG1 and SREBF1 caused by ART were observed not only in the fetus but also in the placenta, primarily in the ICSI group

8. No significant associations were found between polymorphisms of INSIG1 gene and metabolic syndrome; however, INSIG1 and INSIG2 interactions were found in the significant 3-locus and 4-locus gene-gene interaction models.

9. From genetic association studies, SNPs in INSIG1 (including the promoter region) influence hypertriglyceridemia.

10. Common variation in INSIG1 is unlikely to have a major effect on risk of type 2 diabetes risk in white Europeans.

11. These data suggest that p97 recruits proteasomes to polytopic ER proteins, such as Insig-1, even before they are extracted from membranes.

12. INSIG1 and p41 Arp2/3 complex (p41-Arc)reduced expression might be involved in gastric cancer development or progression

13. INSIG-1 plays a role in regulating cholesterol concentration in human cells

14. Data show that Insig-1 appears to play an essential role in the sterol-mediated trafficking of two proteins with sterol-sensing domains, HMG CoA reductase and SCAP.

15. insig-1 expression restricts lipogenesis in mature adipocytes and blocks differentiation in preadipocytes

16. data indicate that short segments at the N and C termini of insulin induced gene 1(Insig-1) face the cytosol with most of the protein buried within the membrane, forming six transmembrane segments

17. nSREBPs are essential for high levels of lipid synthesis in the liver and indicate that Insig's modulate nSREBP levels by binding and retaining SCAP in the ER.

18. Insig-1 has a role in feedback control of lipid synthesis in cultured cells

19. Insig-1 has a role in activation of sterol regulatory element-binding protein induced by cellular stress

20. Insig is required for sterol-mediated inhibition of Scap/SREBP binding to COPII proteins in vitro

Cow (Bovine) Insulin Induced Gene 1 (INSIG1) interaction partners

1. In Nanyang Chinese cattle, seven common haplotypes were identified in the INSIG1 gene based on four coding region SNPs.

Mouse (Murine) Insulin Induced Gene 1 (INSIG1) interaction partners

1. Intracellular biosynthesis of lipids and cholesterol by Scap and Insig in mesenchymal cells regulates long bone growth and chondrocyte homeostasis.

2. myeloid-cell-specific Insig1-/- mice are more susceptible to HSV-1 infection

3. the essential role of Insig1,2 proteins in the sterol homeostasis of enterocytes.

4. reducing Insig1 mRNA to a similar degree observed in morbidly obese human WAT accelerates adipocyte differentiation and enhances lipogenesis, and consequently, lipid accumulation

5. we consistently observe involvement of gp78 in Insig-1 degradation, we find no substantive evidence to support roles for either gp78 or TRC8 in the robust sterol-accelerated degradation of HMG-CoA reductase.

6. analysis of mRNA abundance and expression of SLC27A, ACC, SCD, FADS, LPIN, INSIG, and PPARGC1 gene isoforms in mouse mammary glands during the lactation cycle

7. Insig deficiency in skin causes accumulation of cholesterol precursors, and this impairs normal hair development

8. insig-1 expression restricts lipogenesis in mature adipocytes and blocks differentiation in preadipocytes

9. the regulation of Insig-1 by PPARgamma agonists could in turn regulate SREBP processing and thus couple insulin sensitizers with the regulation of lipid homeostasis

10. Results define Insig proteins 1 and 2 as essential elements of the feedback inhibition system of cholesterol synthesis in mouse liver.

11. IRS2, HK2 and INSIG1 are direct targets of TFE3

12. Treatment of pregnant mice with the HMG-CoA reductase inhibitor lovastatin reduced sterol synthesis in Insig1-knockout embryos and reduced the pre-cholesterol intermediates ameliorating the clefting.

13. Activation of CAR and PXR in mouse liver results in activation of Insig-1 along with reduced protein levels of the active form of sterol regulatory element binding protein 1 (Srebp-1).

14. Insig-1 is a direct PPARdelta target gene in hepatocytes. PPARdelta inhibited SREBP-1 activation via induction of Insig-1. Overexpression of PPARdelta induced the expression of Insig-1, suppressed SREBP-1 activation, and ameliorated hepatic steatosis.

15. Silibinin inhibits adipocyte differentiation through a potential up-regulation of insig-1 and insig-2 at an early phase in adipocyte differentiation.