about
Biologically inactive leptin and early-onset extreme obesity.TNF-related apoptosis-inducing ligand promotes human preadipocyte proliferation via ERK1/2 activation.Severe Early-Onset Obesity Due to Bioinactive Leptin Caused by a p.N103K Mutation in the Leptin GeneMonogenic forms of childhood obesity due to mutations in the leptin geneResveratrol suppresses PAI-1 gene expression in a human in vitro model of inflamed adipose tissue.TRAIL (TNF-related apoptosis-inducing ligand) inhibits human adipocyte differentiation via caspase-mediated downregulation of adipogenic transcription factors.miR-146a-mediated suppression of the inflammatory response in human adipocytes.Measurement of immunofunctional leptin to detect and monitor patients with functional leptin deficiencyTrail (TNF-related apoptosis-inducing ligand) induces an inflammatory response in human adipocytes.Estimated prevalence of potentially damaging variants in the leptin gene.Early childhood BMI trajectories in monogenic obesity due to leptin, leptin receptor, and melanocortin 4 receptor deficiency.Biologically inactive leptin and early-onset extreme obesityFunctional and Phenotypic Characteristics of Human Leptin Receptor MutationsBeyond adiponectin and leptin: adipose tissue-derived mediators of inter-organ communication
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description
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Jan-Bernd Funcke
@ast
Jan-Bernd Funcke
@en
Jan-Bernd Funcke
@es
Jan-Bernd Funcke
@nl
type
label
Jan-Bernd Funcke
@ast
Jan-Bernd Funcke
@en
Jan-Bernd Funcke
@es
Jan-Bernd Funcke
@nl
prefLabel
Jan-Bernd Funcke
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Jan-Bernd Funcke
@en
Jan-Bernd Funcke
@es
Jan-Bernd Funcke
@nl
P106
P31
P496
0000-0002-2596-3167