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Human Polyclonal INSIG2 Primary Antibody pour WB - ABIN4892461
Segatto, Di Giovanni, Marino, Pallottini: Analysis of the protein network of cholesterol homeostasis in different brain regions: an age and sex dependent perspective. dans Journal of cellular physiology 2013
Cow (Bovine) Polyclonal INSIG2 Primary Antibody pour WB - ABIN2778637
Li, Gruidl, Eschrich, McCarthy, Wang, Alexandrow, Yeatman: Insig2 is associated with colon tumorigenesis and inhibits Bax-mediated apoptosis. dans International journal of cancer. Journal international du cancer 2008
Show all 2 Pubmed References
INSIG2 rs10185316 polymorphism was associated with diastolic blood pressure, pulse pressure and mean arterial pressure among children and adolescents in an independent way from body mass index.
IINSIG2 gene single nucleotide polymorphisms and global DNA methylation are linked with weight loss in obese patients.
INSIG2 plays a role in weight gain and obesity during clozapine treatment
These results indicate that HIF-mediated induction of Insig-2 and degradation of HMGCR are physiologically relevant events that guard against wasteful oxygen consumption and inappropriate cell growth during hypoxia.
There may be a connection between INSIG2 expression and metastatic dissemination of colorectal cancer without any effect on tumorigenesis.
Insulin resistance in obese boys leads to up-regulation of INSIG2 gene expression as well as to down-regulation of PFKFB1, PFKFB3, and HK2 genes in the blood cells as compared to obese patients with normal insulin sensitivity.
Results confirmed that genetic variation in INSIG2 is associated with both overweight and LDL in non-Hispanic white children.
This study suggests that the G allele in the INSIG2 single nucleotide polymorphism rs7566605 is more relevant for changes in intramuscular adipose tissue following training than for the amount of subcutaneous fat.
INSIG2 is involved in adipogenesis and MC4R effects hormonal appetite control in response to the amount of adipose tissue.
The results provided evidence for identifying genetic factors of nonalcoholic fatty liver disease (NAFLD) and may be useful for risk assessment and personalized medicine of NAFLD.
The INSIG2 rs7566605 SNP may not play a role in the development of obesity-related metabolic traits in Malaysian Malays.
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.
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.
Results show significant differences in distribution of single nucleotide polymorphism in this gene amongst whites and hispanics
The rs13428113 polymorphism in INSIG2 gene was associated with abnormal lipid metabolism in overweight and obese children.
genetic association/nutrigenomics studies of populations in Samoa: Data suggest that an SNP in INSIG2 (rs9308762) is associated with increased risk of metabolic syndrome X in Samoans eating modern diet (rather than traditional Samoan diet).
In single-marker-based analysis, the INSIG2 rs11123469-C homozygous genotype was found to be more frequent in patients with metabolic syndrome than those without metabolic syndrome.
Single nucleotide polymorphism in INSIG2 is associated with asthma susceptibility through gene-gene interactions.
Results indicated that the G-102A INSIG2 polymorphism has no consistent effect on BMI in general populations, but could influence HDL cholesterol in females.
INSIG2 was significantly associated with fasting plasma glucose in patients with schizophrenia
FASN gene is a promising marker for subcutaneous fat tissue accumulation, while INSIG2 is a promising marker for FA composition
These results suggest that PPARalpha is a trans-acting factor that enhances Insig2a gene expression, thereby suppressing SREBP-1c processing during fasting.
Intracellular biosynthesis of lipids and cholesterol by Scap and Insig in mesenchymal cells regulates long bone growth and chondrocyte homeostasis.
INSIG2 is a negative regulator of SREBP, and acute glucocorticoid treatment decreased active SREBP during refeeding or in livers of Ob/Ob mice, both systems of elevated SREBP-1c-driven lipogenesis.
the essential role of Insig1,2 proteins in the sterol homeostasis of enterocytes.
Insig deficiency in skin causes accumulation of cholesterol precursors, and this impairs normal hair development
Data show that REV-ERBalpha participates in the circadian modulation of SREBP activity, and the expression of SREBP target genes involved in cholesterol and lipid metabolism via the cyclic transcription of Insig2.
Liver-specific mRNA for Insig-2 down-regulated by insulin: implications for fatty acid synthesis.
a vitamin D response element in the murine Insig-2 promoter may have a role in the differentiation of 3T3-L1 preadipocytes
Results define Insig proteins 1 and 2 as essential elements of the feedback inhibition system of cholesterol synthesis in mouse liver.
Insig2 identified as a strong candidate susceptibility gene for total plasma cholesterol levelsin inbred mice strains
Treatment of pregnant mice with the HMG-CoA reductase inhibitor lovastatin reduced sterol synthesis in Insig2-knockout embryos and reduced the pre-cholesterol intermediates ameliorating the clefting.
A critical gene involved in cholesterol homeostasis, Insig-2, was induced when mice or cultured cells were treated with FXRalpha agonists or infected with constitutively active FXRalpha.
Peroxisome deficiency causes a complex phenotype because of hepatic SREBP-1c,-2/Insig-2a,b dysregulation associated with endoplasmic reticulum stress
Silibinin inhibits adipocyte differentiation through a potential up-regulation of insig-1 and insig-2 at an early phase in adipocyte differentiation.
The protein encoded by this gene is highly similar to the protein product encoded by gene INSIG1. Both INSIG1 protein and this protein are endoplasmic reticulum proteins that block the processing of sterol regulatory element binding proteins (SREBPs) by binding to SREBP cleavage-activating protein (SCAP), and thus prevent SCAP from escorting SREBPs to the Golgi.
insulin-induced gene 2 protein
, insulin-induced gene 2 protein-like
, insulin induced gene 2
, INSIG2 membrane protein
, insulin induced protein 2
, insulin-induced membrane protein 2
, INSIG-2 membrane protein
, Insulin-induced gene 2 protein