Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Abnormal neocortex arealization and Sotos-like syndrome-associated behavior in Setd2 mutant mice

ABSTRACT: Abnormal neocortex arealization and Sotos-like syndrome-associated behavior in Setd2 mutant mice

PROVIDER: PRJNA566085 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Abnormal neocortex arealization and Sotos-like syndrome-associated behavior in Setd2 mutant mice

Project description:Abnormal neocortex arealization and Sotos-like syndrome-associated behavior in Setd2 mutant mice

| PRJNA574933 | ENA

Abnormal neocortex arealization and Sotos-like syndrome-associated behavior in Setd2 mutant mice

Project description:Epigenetic regulation of gene expression through histone modifications like methylation of various lysine residues are essential for embryonic development. Here we removed SETD2, a methyltransferase for histone 3 lysine 36 trimethylation (H3K36me3), in the developing dorsal forebrain in mice and show it is required for proper area patterning (arealization) of the neocortex and the formation of thalamo-cortico-thalamic circuits by maintaining the expression of clustered protocadherin (Pcdh) genes in an H3K36me3 methyltransferase-dependent manner. Moreover, the Setd2 mutant mice exhibit defects in social interaction, motor endurance and spatial memory, reminiscent of patients with the Sotos-like syndrome bearing SETD2 mutations.

2020-09-30 | GSE137622 | GEO

Abnormal neocortex arealization and Sotos-like syndrome-associated behavior in Setd2 mutant mice

2020-10-01 | GSE138153 | GEO

Abnormal neocortex arealization and Sotos-like syndrome-associated behavior in <i>Setd2</i> mutant mice.

Project description: Not available

| S-EPMC7775761 | biostudies-literature

Expression data from Sotos syndrome patients and controls

Project description:Genome-wide expression studies were performed on dermal fibroblasts from Sotos syndrome patients with a confirmed NSD1 abnormality and compared with age-sex matched controls. We used microarrays to detect differentially expressed genes in Sotos syndrome patients and performed a global test with the aim to map NSD1 within a signaling transduction pathway. Dermal fibroblasts were obtained from nine Sotos syndrome patients and nine controls. Since NSD1 is a co-factor of the retinoic acid receptor, cultures were performed both in the presence and absence of retinoic acid.

2014-02-06 | E-GEOD-27200 | biostudies-arrayexpress

Metabolic lactate production coordinates vasculature development and progenitor behavior in the developing mouse neocortex

Project description:Proper neural progenitor behavior in conjunction with orderly vasculature formation is fundamental to the development of the neocortex. However, the mechanisms coordinating neural progenitor behavior and vessel growth remain largely elusive. Here we show that robust metabolic production of lactate by radial glial progenitors (RGPs) co-regulates vascular development and RGP division behavior in the developing mouse neocortex. RGPs undergo a highly organized lineage progression program to produce diverse neural progeny. Systematic single cell metabolic state analysis revealed that RGPs and their progeny exhibit distinct metabolic features associated with specific cell types and lineage progression statuses. Symmetrically dividing, proliferative RGPs preferentially express a cohort of genes that support glucose uptake and anaerobic glycolysis. Consequently, they consume glucose in anaerobic metabolism and produce a high level of lactate, which promotes vessel growth. Moreover, lactate production enhances RGP proliferation by maintaining mitochondrial length. Together, these results suggest that specific metabolic states and metabolites coordinately regulate vasculature formation and progenitor behavior in neocortical development.

2022-06-06 | GSE201991 | GEO

Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma [RNA-Seq]

Project description:H3K36me3 catalyzed by histone methyltransferase SETD2 is one of the most conserved epigenetic marks from yeast to mammals. SETD2 is frequently mutated in multiple cancers and acts as a tumor suppressor. Here, utilizing a liver-specific deletion of Setd2 mice model, we found that Setd2 depletion is sufficient to trigger hepatocarcinoma (HCC) spontaneously. Meanwhile, in a DEN-induced HCC model, Setd2 depletion significantly promoted tumor number and size. The mechanistic study showed that Setd2 suppresses HCC not only through modulating DNA damage response, but also regulating lipid metabolism in liver. Setd2 deficiency down-regulated the expression of cholesterol efflux genes and caused lipid accumulation. ChIP-Seq analysis further revealed that Setd2 deletion induced AP-1 activation in liver, which was probably trigged by accumulated cholesterol. AP-1 is a well-known oncogene in HCC and inhibits p53 in Setd2-deficient cells. Taken together, we found the role of an important epigenetic gene in regulating cholesterol homeostasis and HCC, and revealed the underlying mechanisms.

2021-09-01 | GSE136742 | GEO

Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma [ChIP-Seq]

2021-09-01 | GSE136743 | GEO

Pogz deficiency leads to abnormal behavior, transcription dysregulation and impaired cerebellar physiology

Project description:Pogz deficiency leads to abnormal behavior, transcription dysregulation and impaired cerebellar physiology

| PRJNA604449 | ENA

Expression data from Sotos syndrome patients and controls

2014-02-06 | GSE27200 | GEO