Proteomics

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TMT analysis of TBX20:CASZ1 mutant mice with dilated cardiomyopathy


ABSTRACT: Using an unbiased systems-based screen, we demonstrate the cardiac transcription factor TBX20 physically and genetically interacts with the essential transcription factor CASZ1. This interaction is required for survival as mice heterozygous for both Tbx20 and Casz1 die post-natally as a result of dilated cardiomyopathy (DCM).We have used quantitative proteomic approaches to define the molecular pathways mis-regulated in Tbx20 and Casz1 mice and thus, are associated with DCM. Using an unbiased systems-based screen, we demonstrate the cardiac transcription factor TBX20 physically and genetically interacts with the essential transcription factor CASZ1. This interaction is required for survival as mice heterozygous for both Tbx20 and Casz1 die post-natally as a result of dilated cardiomyopathy (DCM).We have used quantitative proteomic approaches to define the molecular pathways mis-regulated in Tbx20 and Casz1 mice and thus, are associated with DCM.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

DISEASE(S): Dilated Cardiomyopathy

SUBMITTER: Todd Greco  

LAB HEAD: Ileana Cristea

PROVIDER: PXD005788 | Pride | 2022-05-27

REPOSITORIES: Pride

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Publications

Formation of a TBX20-CASZ1 protein complex is protective against dilated cardiomyopathy and critical for cardiac homeostasis.

Kennedy Leslie L   Kaltenbrun Erin E   Greco Todd M TM   Temple Brenda B   Herring Laura E LE   Cristea Ileana M IM   Conlon Frank L FL  

PLoS genetics 20170925 9


By the age of 40, one in five adults without symptoms of cardiovascular disease are at risk for developing congestive heart failure. Within this population, dilated cardiomyopathy (DCM) remains one of the leading causes of disease and death, with nearly half of cases genetically determined. Though genetic and high throughput sequencing-based approaches have identified sporadic and inherited mutations in a multitude of genes implicated in cardiomyopathy, how combinations of asymptomatic mutations  ...[more]

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