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Articles by Decheng Ren
Identification of Schizophrenia‐Risk Regulatory Variant rs1399178 in the Non‐coding Region With Its Impact on NRF1 Binding
1 Introduction Schizophrenia, considered one of the most severe mental disorders, is a chronic psychiatric condition with a diverse genetic and neurobiological foundation that impacts early brain development [1]. Schizophrenia is usually characterized as a combination of psychotic symptoms, including delusions, hallucinations, disordered thought, and reduced emotional expression [2, 3].
TULP4, a novel E3 ligase gene, participates in neuronal migration as a candidate in schizophrenia
1 INTRODUCTION Schizophrenia is a debilitating psychiatric disorder with a well-established genetic1 and neurobiological background2 that impacts early brain development. Genetic studies of schizophrenia have confirmed a substantial heritability that reflects common and rare alleles at numerous loci.3 Compared with common variants, rare variants often result in more direct functional abnormalities,4 making them more amenable to molecular mechanistic studies.
Adipose METTL14‐Elicited N6‐Methyladenosine Promotes Obesity, Insulin Resistance, and NAFLD Through Suppressing β Adrenergic Signaling and Lipolysis
1 Introduction Excessive expansion of white adipose tissue (WAT), a hallmark of obesity, is a risk factor for metabolic disease, and the underlying mechanism is complex and poorly understood.
Adipose METTL14‐Elicited N6‐Methyladenosine Promotes Obesity, Insulin Resistance, and NAFLD Through Suppressing β Adrenergic Signaling and Lipolysis
1 Introduction Excessive expansion of white adipose tissue (WAT), a hallmark of obesity, is a risk factor for metabolic disease, and the underlying mechanism is complex and poorly understood.
Critical role for the Tsc1-mTORC1 pathway in β-cell mass in Pdx1-deficient mice
Pdx1 (pancreas and duodenal homeobox-1) plays an essential role in pancreas development, β-cell function and survival. Islet-specific disruption of Pdx1 causes impaired insulin release, glucose intolerance and diabetes ( Ahlgren et al. 1998 , Johnson et al. 2003 ). Humans with heterozygous missense and frame shift mutations of the Pdx1 gene develop reductions in insulin secretion resulting in one form of maturity-onset diabetes of the young (MODY 4).
Critical role for the Tsc1-mTORC1 pathway in β-cell mass in Pdx1-deficient mice
Mutations in the pancreatic duodenal homeobox (PDX1) gene are associated with diabetes in humans. Pdx1-haploinsufficient mice also develop diabetes, but the molecular mechanism is unknown. To this end, we knocked down Pdx1 gene expression in mouse MIN6 insulinoma cells. Pdx1 suppression not only increased apoptotic cell death but also decreased cell proliferation, which was associated with a decrease in activity of mechanistic target of rapamycin complex 1 (mTORC1).
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