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SIM1 and SIM2 genes are Drosophila single-minded (sim) gene homologs. Additionally we are shipping SIM1 Antibodies (40) and many more products for this protein.
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Genotype-phenotype correlations confirmed the major role for SIM1 haploinsufficiency in obesity and the Prader-Willi-like phenotype
Aberrant DNA methylation (show HELLS Proteins) of the DLX4 (show DLX4 Proteins) and SIM1 genes may be a novel progression marker for uterine cervical low-grade squamous intraepithelial lesions.
Severe loss-of-function SIM1 mutations can be associated with a spectrum of developmental delay phenotypes and obesity.
functional in vitro analysis of SIM1 variants may help in distinguishing benign variants of no pathogenic significance from variants which contribute to the obesity phenotype.
Study found a statistically significant association between the SIM1 SNP rs3734354 (Pro352Thr) and scores for language impairment (p = .0004), but due to low statistical power this should be interpreted cautiously
two brain enhancers in the SIM1 locus are characterized with a set of obesity-specific SNPs within one of them, which may predispose individuals to obesity.
Data suggest selected SIM1 variants exhibit poor dimerization with ARNT2 (aryl-hydrocarbon receptor nuclear translocator 2 (show ARNT2 Proteins)) and anomalous intracellular localization; data were used to predict spot in SIM1/SIM2 (show SIM2 Proteins) (residues 290-326) critical in function.
Hence, we suggest that detailed endocrine evaluation and longitudinal endocrine follow up be performed in individuals with proximal interstitial 6q deletion involving SIM1
A link between SIM1 loss of function and severe obesity associated with, or independent of, Prader-Willi-like features.
Phenotypic similarities between patients with SIM1 deficiency and MC4R (show MC4R Proteins) deficiency suggest that some of the effects of SIM1 deficiency on energy homeostasis are mediated by altered melanocortin signaling.
Results demonstrate that Sim1 is essential for proper migration and the guidance of commissural axons of the spinal V3 interneurons
These findings reveal Sim1 as a critical yet previously unrecognized modulator of skeletal homeostasis that functions through a central relay.
CB1 (show CNR1 Proteins) receptors on Sim1-positive neurons do not impact food intake but hinder energy expenditure during dietary environmental challenges that promote body weight gain.
Results show that Sim1 acts physiologically as well as developmentally to regulate body weight.
Paraventricular nucleus Sim1 neuron ablation mediated obesity is resistant to high fat diet.
Sim1 neurons in adult mice regulate both food intake and energy expenditure
Sim1 is a regulator of dorsal raphe nucleus specification acting upstream of Pet1 (show FEV Proteins) and Tph2 (show TPH2 Proteins).
Sim1 haploinsufficiency is thus associated with a decrease of several paraventricular nucleus and supraoptic nucleus of the hypothalamus cell types, which has the potential of affecting distinct homeostatic processes.
Differential activities of murine single minded 1 (SIM1) and SIM2 (show SIM2 Proteins) on a hypoxic response element
interaction between SIM1 and arylhydrocarbon receptor involved in the control of food intake
three SIM1 genotypes (CC, CT, TT) were found and their frequencies between domestic and foreign breeds were different
SIM1 and SIM2 genes are Drosophila single-minded (sim) gene homologs. SIM1 transcript was detected only in fetal kidney out of various adult and fetal tissues tested. Since the sim gene plays an important role in Drosophila development and has peak levels of expression during the period of neurogenesis,it was proposed that the human SIM gene is a candidate for involvement in certain dysmorphic features (particularly the facial and skull characteristics), abnormalities of brain development, and/or mental retardation of Down syndrome.
class E basic helix-loop-helix protein 14
, single-minded homolog 1
, single-minded 1
, single-minded-like 1