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mitochondria-associated protein catabolic process

Known as: mitochondrion-associated protein catabolic process, mitochondria-associated protein degradation, MAD 
The chemical reactions and pathways resulting in the breakdown of proteins transported from mitochondria and targeted to cytoplasmic proteasomes for… Expand
National Institutes of Health

Papers overview

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Review
2011
Review
2011
Mitochondrial quality control by the ubiquitin-proteasome system.
Mitochondria perform multiple functions critical to the maintenance of cellular homoeostasis and their dysfunction leads to… Expand
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Highly Cited
2003
Highly Cited
2003
dSmurf Selectively Degrades Decapentaplegic-activated MAD, and Its Overexpression Disrupts Imaginal Disc Development*
MAD plays an important role in decapentaplegic (DPP) signaling throughout Drosophila development. Despite a recent study… Expand
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Review
2001
Review
2001
The interplay between Mad and Myc in proliferation and differentiation.
Members of the Myc family of transcription factors are key regulators of cell proliferation, and excessive levels of Myc lead to… Expand
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Highly Cited
1997
Highly Cited
1997
The MAD-related protein Smad7 associates with the TGFbeta receptor and functions as an antagonist of TGFbeta signaling.
TGFbeta signaling is initiated when the type I receptor phosphorylates the MAD-related protein, Smad2, on C-terminal serine… Expand
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Highly Cited
1997
Highly Cited
1997
Vascular MADs: two novel MAD-related genes selectively inducible by flow in human vascular endothelium.
Vascular endothelium is an important transducer and integrator of both humoral and biomechanical stimuli within the… Expand
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Highly Cited
1995
Highly Cited
1995
Effects of the MYC oncogene antagonist, MAD, on proliferation, cell cycling and the malignant phenotype of human brain tumour cells
To investigate how overexpression of MAD, an antagonist of MYC oncogenes influences the malignant phenotype of human cancer cells… Expand
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Highly Cited
1995
Highly Cited
1995
Differential effects by Mad and Max on transformation by cellular and viral oncoproteins.
c-Myc is an essential component of the regulatory mechanisms controlling cell growth. Max is the obligatory partner of c-Myc for… Expand
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Highly Cited
1994
Highly Cited
1994
Suppression of Myc, but not E1a, transformation activity by Max-associated proteins, Mad and Mxi1.
Mad and Mxi1, two members of the Myc-related basic-region helix-loop-helix/leucine-zipper family of proteins, associate directly… Expand
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Highly Cited
1994
Highly Cited
1994
Mapping of two genes encoding members of a distinct subfamily of MAX interacting proteins: MAD to human chromosome 2 and mouse chromosome 6, and MXI1 to human chromosome 10 and mouse chromosome 19.
Both the MAD and the MXI1 genes encode basic-helix-loop-helix-leucine zipper (bHLH-Zip) transcription factors which bind Max in… Expand
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Highly Cited
1986
Highly Cited
1986
The multiple acyl-coenzyme A dehydrogenation disorders, glutaric aciduria type II and ethylmalonic-adipic aciduria. Mitochondrial fatty acid oxidation, acyl-coenzyme A dehydrogenase, and electron…
The multiple acyl-coenzyme A (CoA) dehydrogenation disorders (MAD) include severe (S) and mild (M) variants, glutaric aciduria… Expand
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