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Proteasome-Mediated Processing of Nrf1 Is Essential for Coordinate Induction of All Proteasome Subunits and p97

Current biology, 2014-07, Vol.24 (14), p.1573-1583

2014

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The Logic of the 26S Proteasome

Cell, 2017-05, Vol.169 (5), p.792-806

2017

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Development of proteasome inhibitors as research tools and cancer drugs

The Journal of cell biology, 2012-11, Vol.199 (4), p.583-588

Goldberg, Alfred L

2012

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Muscle wasting in disease: molecular mechanisms and promising therapies

Nature reviews. Drug discovery, 2015-01, Vol.14 (1), p.58-74

2015

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SIRT1 Protein, by Blocking the Activities of Transcription Factors FoxO1 and FoxO3, Inhibits Muscle Atrophy and Promotes Muscle Growth

The Journal of biological chemistry, 2013-10, Vol.288 (42), p.30515-30526

2013

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The deubiquitinating enzyme Usp14 allosterically inhibits multiple proteasomal activities and ubiquitin-independent proteolysis

The Journal of biological chemistry, 2017-06, Vol.292 (23), p.9830-9839

2017

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UBL domain of Usp14 and other proteins stimulates proteasome activities and protein degradation in cells

Proceedings of the National Academy of Sciences - PNAS, 2018-12, Vol.115 (50), p.E11642-E11650

2018

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Regulating protein breakdown through proteasome phosphorylation

Biochemical journal, 2017-10, Vol.474 (19), p.3355-3371

2017

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Acetylation-Mediated Proteasomal Degradation of Core Histones during DNA Repair and Spermatogenesis

Cell, 2013-05, Vol.153 (5), p.1012-1024

2013

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ZFAND5/ZNF216 is an activator of the 26S proteasome that stimulates overall protein degradation

Proceedings of the National Academy of Sciences - PNAS, 2018-10, Vol.115 (41), p.E9550-E9559

2018

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Regulation of autophagy and the ubiquitin-proteasome system by the FoxO transcriptional network during muscle atrophy

Nature communications, 2015-04, Vol.6 (1), p.6670-6670, Article 6670

2015

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26S proteasomes become stably activated upon heat shock when ubiquitination and protein degradation increase

Proceedings of the National Academy of Sciences - PNAS, 2022-06, Vol.119 (25), p.e2122482119-e2122482119

2022

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Multiple myeloma cells are exceptionally sensitive to heat shock, which overwhelms their proteostasis network and induces apoptosis

Proceedings of the National Academy of Sciences - PNAS, 2020-09, Vol.117 (35), p.21588-21597

2020

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Proteins containing ubiquitin-like (Ubl) domains not only bind to 26S proteasomes but also induce their activation

Proceedings of the National Academy of Sciences - PNAS, 2020-03, Vol.117 (9), p.4664-4674

2020

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Protein degradation and protection against misfolded or damaged proteins

Nature (London), 2003-12, Vol.426 (6968), p.895-899

Goldberg, Alfred L

2003

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ATP-Dependent Steps in the Binding of Ubiquitin Conjugates to the 26S Proteasome that Commit to Degradation

Molecular cell, 2010-11, Vol.40 (4), p.671-681

2010

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The influence of skeletal muscle on systemic aging and lifespan

Aging cell, 2013-12, Vol.12 (6), p.943-949

2013

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Coordinate regulation of autophagy and the ubiquitin proteasome system by MTOR

Autophagy, 2016-10, Vol.12 (10), p.1967-1970

2016

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Myostatin/activin pathway antagonism: Molecular basis and therapeutic potential

The international journal of biochemistry & cell biology, 2013-10, Vol.45 (10), p.2333-2347

2013

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Immuno- and Constitutive Proteasomes Do Not Differ in Their Abilities to Degrade Ubiquitinated Proteins

Cell, 2013-02, Vol.152 (5), p.1184-1194

2013

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Protein degradation by the ubiquitin-proteasome pathway in normal and disease states

Journal of the American Society of Nephrology, 2006-07, Vol.17 (7), p.1807-1819

2006

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Ubiquitylation by Trim32 causes coupled loss of desmin, Z-bands, and thin filaments in muscle atrophy

The Journal of cell biology, 2012-08, Vol.198 (4), p.575-589

2012

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Tau-driven 26S proteasome impairment and cognitive dysfunction can be prevented early in disease by activating cAMP-PKA signaling

Nature medicine, 2016-01, Vol.22 (1), p.46-53

2016

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Mycobacterium tuberculosis ClpP1 and ClpP2 function together in protein degradation and are required for viability in vitro and during infection

PLoS pathogens, 2012-02, Vol.8 (2), p.e1002511-e1002511

2012

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Muscle Wasting in Fasting Requires Activation of NF-κB and Inhibition of AKT/Mechanistic Target of Rapamycin (mTOR) by the Protein Acetylase, GCN5

The Journal of biological chemistry, 2015-12, Vol.290 (51), p.30269-30279

2015

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Proteasome-Mediated Processing of Nrf1 Is Essential for Coordinate Induction of All Proteasome Subunits and p97

The Logic of the 26S Proteasome

Development of proteasome inhibitors as research tools and cancer drugs

Muscle wasting in disease: molecular mechanisms and promising therapies

SIRT1 Protein, by Blocking the Activities of Transcription Factors FoxO1 and FoxO3, Inhibits Muscle Atrophy and Promotes Muscle Growth

The deubiquitinating enzyme Usp14 allosterically inhibits multiple proteasomal activities and ubiquitin-independent proteolysis

UBL domain of Usp14 and other proteins stimulates proteasome activities and protein degradation in cells

Regulating protein breakdown through proteasome phosphorylation

Acetylation-Mediated Proteasomal Degradation of Core Histones during DNA Repair and Spermatogenesis

ZFAND5/ZNF216 is an activator of the 26S proteasome that stimulates overall protein degradation

Regulation of autophagy and the ubiquitin-proteasome system by the FoxO transcriptional network during muscle atrophy

26S proteasomes become stably activated upon heat shock when ubiquitination and protein degradation increase

Multiple myeloma cells are exceptionally sensitive to heat shock, which overwhelms their proteostasis network and induces apoptosis

Proteins containing ubiquitin-like (Ubl) domains not only bind to 26S proteasomes but also induce their activation

Protein degradation and protection against misfolded or damaged proteins

ATP-Dependent Steps in the Binding of Ubiquitin Conjugates to the 26S Proteasome that Commit to Degradation

The influence of skeletal muscle on systemic aging and lifespan

Coordinate regulation of autophagy and the ubiquitin proteasome system by MTOR

Myostatin/activin pathway antagonism: Molecular basis and therapeutic potential

Immuno- and Constitutive Proteasomes Do Not Differ in Their Abilities to Degrade Ubiquitinated Proteins

Protein degradation by the ubiquitin-proteasome pathway in normal and disease states

Ubiquitylation by Trim32 causes coupled loss of desmin, Z-bands, and thin filaments in muscle atrophy

Tau-driven 26S proteasome impairment and cognitive dysfunction can be prevented early in disease by activating cAMP-PKA signaling

Mycobacterium tuberculosis ClpP1 and ClpP2 function together in protein degradation and are required for viability in vitro and during infection

Muscle Wasting in Fasting Requires Activation of NF-κB and Inhibition of AKT/Mechanistic Target of Rapamycin (mTOR) by the Protein Acetylase, GCN5

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