Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Temporalis Left

ABSTRACT: Temporalis Left muscle

SUBMITTER: David Nickerson

PROVIDER: 994 | Physiome Model Repository |

REPOSITORIES: PMR

ACCESS DATA

Json Xml

Publications

Sorry, this publication's infomation has not been loaded in the Indexer, please go directly to PUBMED or Altmetric.

Similar Datasets

Gene expression in rabbit left atrial free wall and left atrial appendage

Project description:Gene expression in rabbit left atrial free wall and left atrial appendage

| PRJNA483207 | ENA

Adult rabbit left ventricle RNAseq

Project description:Adult rabbit left ventricle RNAseq

| PRJNA475561 | ENA

RNA-seq of heart left ventricle

Project description:RNA-seq of heart left ventricle

| PRJNA549694 | ENA

Colonic Crohn's left and right colon

Project description:Colonic Crohn's left and right colon

| PRJNA593867 | ENA

Gene expression in rabbit left atrial free wall and left atrial appendage

Project description:RNA sequencing of dissected left atrial free wall and left atrial appendage of adult New Zealand White rabbit

2018-10-19 | GSE117801 | GEO

Sequential defects in cardiac lineage commitment and maturation cause hypoplastic left heart syndrome

Project description:Complex molecular programs in specific cell lineages govern human heart development. Hypoplastic left heart syndrome (HLHS) is the most severe congenital heart defect encompassing a spectrum of left-ventricular hypoplasia occurring in association with outflow-tract obstruction. The current clinical paradigm assumes HLHS is largely of hemodynamic origin. Here, by combining whole-exome sequencing of 87 HLHS parent-offspring trios and transcriptome of cardiomycytes (CMs) from healthy and patient native ventricles at different stages of development we identified perturbations in coherent gene programs controlling ventricular muscle lineage development. Single-cell and 3D molecular/functional modeling with iPSCs demonstrated intrinsic defects in the cell-cycle/ciliogenesis/autophagy hub resulting in disrupted differentiation of early cardiac progenitor (CP) lineages and ultimate defective CM-subtype differentiation/maturation in HLHS. Moreover, premature cellcycle exit of ventricular CM prevents tissue response to cues of developmental growth leading to multinucleation/polyploidy, accumulation of DNA damage, exacerbated apoptosis, and eventually ventricle hypoplasia. Our results highlight how genetic heterogeneity in HLHS converges in perturbations of sequential cellular processes driving cardiogenesis and facilitate potential novel nodes for therapy beside surgical intervention.

2022-02-15 | PXD014812 | Pride

Masseter Left

Project description:Masseter Left muscle

| 98f | Physiome Model Repository

Ribo-seq of murine left ventricular tissues

Project description:Ribo-seq of murine left ventricular tissues

| PRJEB35636 | ENA

TBX5 Adult Knockout Left Atrial Gene Expression

Project description:TBX5 Adult Knockout Left Atrial Gene Expression

| PRJNA531601 | ENA

microRNA counts from heart left ventricle (ENCSR425ZMS)

Project description:microRNA counts from heart left ventricle (ENCSR425ZMS)