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Adiponectin and adiponectin receptor genes are coexpressed during zebrafish embryogenesis and regulated by food deprivation
Human diabetic kidneys show decreased intraglomerular AdipoR1/AdipoR2 expression.
Based on crystal structure of AdipoR1, we designed AdipoR1's peptide agonists using protein-peptide docking simulation and screened their receptor binding abilities and biological functions via surface plasmon resonance (SPR) and biological analysis
Serum levels of APN and AdipoR1 are significantly lower in type 2 diabetes mellitus (T2DM) group and T2DM + macrovascular complications (MVC) group, showing lowest value in T2DM + MVC group. APN and AdipoR1 levels may influence glucose and lipid metabolism in T2DM patients.
Upregulation of ADIPOR1 and SPP1, among the adipokine gene family, in cancer tissue is associated with poor survival in CRC, suggesting a potential mechanism linking obesity and colorectal cancer.
ADIPOR1 was consistently associated with diabetes and hypertriglyceridemia in an admixed Latin American population.
miR-221 acts as a promoter of the EMT process in HCC cells by targeting AdipoR1
The pathways related to tumorigenicity and tumor progression, STAT2 and AdipoR1/AMPK/SIRT1 could be restrained by miR-3908. In conclusion, restoration of miR-3908 expression induced suppression of cancer progression and glioblastoma tumorigenicity.
Review/Meta-analysis: genetic polymorphisms in leptin, adiponectin and their receptors affect the development and progression of prostate cancer.
Renoprotection of adiponectin is associated with improvement of the endothelial dysfunction, reduction of oxidative stress, and upregulation of endothelial nitric oxide synthase expression through activation of adenosine 5'-monophosphate-activated protein kinase by AdipoR1 and activation of peroxisome proliferator-activated receptor (PPAR)-alpha signaling pathway by AdipoR2. [review]
High ADIPOR1 expression is associated with breast cancer.
revised ADIPOR1 crystal structure exhibiting a seven-transmembrane-domain architecture that is clearly distinct from that of ADIPOR2
TNF-alpha impairs adiponectin/AdipoR1 signaling, mitochondrial biogenesis, and myogenesis in primary human myotubes cultures obtained from heart failure patients.
the knockdown phenotype was partially rescued by injecting wild-type, but not mutant, human ADIPOR1 mRNA. We conclude that ADIPOR1 is a novel adRP-causing gene and plays an important role in rod development and maintenance.
Adiponectin stimulates cPLA2 and COX-2 expression via AdipoR1/2-dependent activation of PKC/NADPH oxidase/mitochondria resulting in ROS accumulation, p300 phosphorylation, and histone H4 acetylation.
Decreased expression of ADIPOR1 is associated with polycystic ovary syndrome.
sequence- and structure-based computational tools were employed in this study to functionally and structurally characterize the coding Nonsynonymous Single Nucleotide Polymorphisms of ADIPOR1 gene listed in the single nucleotide polymorphisms database.
PCR results showed expression of adiponectin, AdipoR1, AdipoR2, follicle-stimulating hormone receptor (FSHR), and luteinizing hormone receptor (LHR) in granulosa cells (GCs). After controlling body mass index (BMI) values, qRT-PCR demonstrated a decreased expression of adiponectin system in GCs of polycystic ovary syndromepatients compared to those in controls
ADPOR1 variants, rs3737884*G and rs7514221*C, may be shared risk factors associated with CAD, T2D, and T2D with CAD in a population of northeast China.
Expression of AdipoR1 gene receptor was increased in endometriotic stromal cells.
miR-323 may increase VEGF-A-mediated cancer vascularization in PC cells through AdipoR1 suppression.
AdipoR1 knockdown mice exhibited increased body weight and abnormal plasma chemistry, and also showed spatial learning and memory impairment in behavioral studies.
ADIPOR activation restores AMPK (AMP-activated protein kinase)-mediated autophagosome formation and antioxidant-mediated autophagosome clearance, representing a novel intervention effective against myocardial ischemia-reperfusion injury in diabetic conditions.
these results demonstrate that AdipoR1 and AdipoR2 exhibit overlapping and distinct effects in skeletal muscle consistent with enhanced adiponectin sensitivity but these appear insufficient to ameliorate established obesity-induced adiponectin resistance.
miR-323-3p appears to be a crucial diabetes factor that mediates its functions by inhibiting the AdipoR1/AMPK/SIRT-1 signaling pathway.
although the physiological levels of adiponectin are sufficient to activate AMPK and Akt when AdipoR1 is overexpressed in beta-cells, yet adiponectin cannot protect beta-cells in Akita mice from ER stress-induced destruction
Immunofluorescence indicated that GPRC6A and adiponectin receptor 1 were co-localized in mouse muscle tissues. The present finding suggested adiponectin receptor 1 can mediate the improvement of glucose metabolism by osteocalcin in ovariectomized mice
adiponectin maintains intestinal homeostasis and protects against murine colitis through interactions with its receptor AdipoR1 and by modulating adaptive immunity and STAT3 signaling
Based on these findings, this study showed that CTRP9 might induce mitochondrial biogenesis and protect high glucose-induced endothelial oxidative damage via AdipoR1-SIRT1-PGC-1alpha signaling pathway.
High salt is an important suppressor of cardioprotective APN and AdipoR1 in cardiac myocytes.
AdipoR1, not AdipoR2, was first identified as a receptor of CTRP6 during the process of mitotic clonal expansion. Collectively, we suggest that CTRP6 mediates the ectopic lipogenesis through AdipoR1/Erk/PPARgamma signaling pathway in myoblasts.
The results demonstrated a dynamic dysfunction of APN/AdipoR1 axis accompanying progression of diabetes mellitus in mice with cerebral ischemia.
physiologic adiponectin levels enhance the vasorelaxative response to acetylcholine by inducing nitric oxide production through AdipoR1/Cav-1 mediated signaling.
AdipoR1 is expressed on adipose tissue-resident Tregs, mainly Helios(+) Tregs, and this expression is dependent on weight and fat accumulation. This data proposes a new mechanism through which weight gain might alter immunoregulation.
Adiponectin directly acts on murine dermal gammadelta-T cells to suppress IL-17 synthesis via AdipoR1.
At high glucose concentrations in vitro, AdipoR1 regulated the survival of neural stem cells through the p53/p21 pathway and the proliferation- and differentiation-related factors of neural stem cells via TLX.
Electroacupuncture induces protective effects against cerebral ischemia through AdipoR1-mediated phosphorylation of GSK-3Beta.
lack of AdipoR1 impairs myocardial mitochondrial function and coupling, suggesting that impaired AdipoR1 signaling may contribute to mitochondrial dysfunction and mitochondrial uncoupling in Type 2 diabetic hearts.
AdipoR1 overexpression in retinal pigment epithelium cells enhances docosahexaenoic acid uptake, whereas AdipoR1 silencing has the opposite effect.
AdipoR1 as a Potential Target for Reversing Diabetes-Induced Osteopenia.
CTRP9 protects against acute cardiac damage in response to pathological stimuli by suppressing inflammatory reactions through AdipoR1/AMPK-dependent mechanisms.
This study demonstrated the presence of adiponectin and its receptors in the uteri, conceptuses, and trophoblasts of pregnant pigs and that the local adiponectin system is dependent on the stage of pregnancy.
Data suggest AdipoR1/adiponectin signaling up-regulates gene expression of hepatocyte enzymes involved in fatty acid metabolism and protects hepatocyte from nonesterified fatty acids by activating phosphatidylinositol 3-kinase (PI3K/AKT) signaling.
study demonstrated that adiponectin and adiponectin receptors 1 and 2 messenger RNAs and proteins are present in the porcine hypothalamus and that their expression levels are determined by the pig's endocrine status related to the oestrous cycle
This study demonstrated the presence of adiponectin, AdipoR1 and AdipoR2 genes and proteins in the porcine uterus and the effect of the stage of the oestrous cycle on the expression of the adiponectin system.
Data indicate that AdipoR1 and AdipoR2 mRNAs and proteins are present in the porcine pituitary and that adiponectin receptors expression is dependent on endocrine status of the animals.
Results showed a high polymorphism of the ADIPOR1 and a complexity in its transcription level in longissimus dorsi from five pig breeds: Duroc, Polish Large White, Polish Landrace, Pietrain and Pulawska.
The cloning and characterization of adiponectin, ADIPOR1, and ADIPOR2 are reported.
FISH localization of 4 BAC clones harbouring potential candidate genes for fatness traits: DGAT1 (SSC4p15), PPARA (SSC5p15), ADIPOR1 (SSC10p13) and CREB (SSC15q24)
Insulin regulates the expression of adiponectin and adiponectin receptors in porcine adipocytes.
SNPs and haplotypes that are associated with large litter size, fewer stillborn and mummified piglets and shorter weaning-to-oestrus intervals.
Low level expression of adiponectin mRNA was found in all areas of bovine mammary gland tissues examined. AdipoR1 and AdipoR2 mRNAs were also detected in mammary tissues and their expression was particularly prominent in the parenchyma and cistern.
The physiologic status of the ovary has significant effects on the natural expression patterns of adiponectin and its receptors in follicular and luteal cells of bovine ovary.
This gene encodes a protein which acts as a receptor for adiponectin, a hormone secreted by adipocytes which regulates fatty acid catabolism and glucose levels. Binding of adiponectin to the encoded protein results in activation of an AMP-activated kinase signaling pathway which affects levels of fatty acid oxidation and insulin sensitivity. A pseudogene of this gene is located on chromosome 14.
adiponectin receptor 1
, adiponectin receptor type I
, adiponectin receptor protein 1
, progestin and adipoQ receptor family member I
, adiponectin receptor protein 1-like