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accession-icon GSE16083
Accelerated Postnatal Growth Increases Lipogenic Gene Expression and Adipocyte Size in Low-Birth Weight Mice
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

OBJECTIVE: To characterize the hormonal milieu and adipose gene expression in response to catch-up growth (CUG), a growth pattern associated with obesity and diabetes risk, in a mouse model of low birth weight (LBW). RESEARCH DESIGN AND METHODS: ICR mice were food restricted by 50% from gestational days 12.5-18.5, reducing offspring birth weight by 25%. During the suckling period, dams were either fed ad libitum, permitting CUG in offspring, or food restricted, preventing CUG. Offspring were killed at age 3 weeks, and gonadal fat was removed for RNA extraction, array analysis, RT-PCR, and evaluation of cell size and number. Serum insulin, thyroxine (T4), corticosterone, and adipokines were measured.

Publication Title

Accelerated postnatal growth increases lipogenic gene expression and adipocyte size in low-birth weight mice.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE66766
Effect of Mut heterozygosity in skeletal muscle gene expression
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Branched-chain amino acids (BCAA) have emerged as predictors of type 2 diabetes (T2D). However, their potential role in the pathogenesis of insulin resistance and T2D remains unclear. By integrating data from skeletal muscle gene expression and metabolomic analyses, we demonstrate evidence for perturbation in BCAA metabolism and fatty acid oxidation in skeletal muscle from insulin-resistant humans. Experimental modulation of BCAA flux in cultured cells alters fatty acid oxidation in parallel. Furthermore, heterozygosity for the BCAA metabolic enzyme methylmalonyl-CoA mutase (MUT) alters muscle lipid metabolism in vivo, resulting in increased muscle triacylglycerol (TAG) accumulation and increased body weight after high-fat feeding. Together, our results demonstrate that impaired muscle BCAA catabolism may contribute to the development of insulin resistance by reducing fatty acid oxidation and increasing TAG accumulation.

Publication Title

Defects in muscle branched-chain amino acid oxidation contribute to impaired lipid metabolism.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon SRP094694
TET2 loss and the lymphoma-associated RHOA mutation cooperate to disrupt CD4+ T cell function through inactivation of FOXO1
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Angioimmunoblastic T cell lymphoma (AITL) represents a distinctive form of peripheral T cell lymphoma with a dismissal prognosis. Recent exome sequencing in AITL patients revealed frequent coexistence of somatic mutations in the RHO GTPase (RHOAG17V) and the 5-methylcytosine oxidase TET2. Here we demonstrated that Tet2 loss and RhoAG17V cooperatively caused abnormal CD4+ T cell proliferation and differentiation by perturbing FoxO1 gene expression and its subcellular localization, an abnormality that is also detected in AITL tumor samples. Re-expression of FoxO1 attenuated aberrant immune responses induced by genetic lesions in both Tet2 and RhoA. Our findings suggest that mutational cooperativity between epigenetic factors and GTPases in adult CD4+ T cells may account for immunoinflammatory responses that are commonly associated with AITL. Overall design: Determine the differential expressed genes between WT, Tet2-/-, RhoAG17V, Tet2-/-RhoAG17V mutant CD4+ T cells.

Publication Title

Mutations in 5-methylcytosine oxidase TET2 and RhoA cooperatively disrupt T cell homeostasis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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