D-Index & Metrics Best Publications
Research.com 2022 Best Scientist Award Badge

D-Index & Metrics

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Biology and Biochemistry D-index 167 Citations 102,547 399 World Ranking 38 National Ranking 33
Best Scientists D-index 181 Citations 116,272 482 World Ranking 414 National Ranking 275

Research.com Recognitions

Awards & Achievements

2022 - Research.com Best Scientist Award

2015 - Member of the National Academy of Sciences

2009 - Fellow of the American Association for the Advancement of Science (AAAS)

2009 - Member of the National Academy of Medicine (NAM)

2007 - Fellow of the American Psychological Association (APA)

2005 - Fellow of the American Academy of Arts and Sciences

Overview

What is he best known for?

The fields of study he is best known for:

  • Enzyme
  • Gene
  • Biochemistry

The scientist’s investigation covers issues in Biochemistry, Proteasome, Protein degradation, Cell biology and Proteolysis. His Biochemistry research focuses on Epitope and how it relates to Peptide. The concepts of his Proteasome study are interwoven with issues in Cell, Ubiquitin, Function and Enzyme.

While the research belongs to areas of Protein degradation, Alfred L. Goldberg spends his time largely on the problem of Muscle atrophy, intersecting his research to questions surrounding Regulation of gene expression, Gene expression, FOXO3 and Ubiquitin ligase. Alfred L. Goldberg combines subjects such as Autophagy, Immune system, Molecular biology, Messenger RNA and Proteasome complex with his study of Cell biology. The Proteolysis study combines topics in areas such as Proteases, Hsp70 and Adenosine triphosphate.

His most cited work include:

  • Foxo Transcription Factors Induce the Atrophy-Related Ubiquitin Ligase Atrogin-1 and Cause Skeletal Muscle Atrophy (2183 citations)
  • Inhibitors of the proteasome block the degradation of most cell proteins and the generation of peptides presented on MHC class I molecules (2179 citations)
  • Structure and Functions of the 20S and 26S Proteasomes (2167 citations)

What are the main themes of his work throughout his whole career to date?

Biochemistry, Proteasome, Protein degradation, Cell biology and Ubiquitin are his primary areas of study. Proteolysis, Protease, Enzyme, ATPase and Proteases are the primary areas of interest in his Biochemistry study. His research investigates the link between Proteasome and topics such as Antigen presentation that cross with problems in MHC class I and Major histocompatibility complex.

His Protein degradation research integrates issues from Endocrinology, Internal medicine, Skeletal muscle, Protein catabolism and Protein biosynthesis. His Skeletal muscle research is multidisciplinary, relying on both Protein turnover and Atrophy. His Cell biology study combines topics from a wide range of disciplines, such as Autophagy and Cell.

He most often published in these fields:

  • Biochemistry (59.26%)
  • Proteasome (38.07%)
  • Protein degradation (27.57%)

What were the highlights of his more recent work (between 2008-2020)?

  • Proteasome (38.07%)
  • Cell biology (26.34%)
  • Ubiquitin (22.84%)

In recent papers he was focusing on the following fields of study:

Alfred L. Goldberg mostly deals with Proteasome, Cell biology, Ubiquitin, Biochemistry and Protein degradation. His research in Proteasome intersects with topics in Autophagy, ATP hydrolysis, Protein subunit, Proteolysis and Phosphorylation. In his research, mTORC1 is intimately related to Amino acid, which falls under the overarching field of Proteolysis.

His studies in Cell biology integrate themes in fields like Protein ubiquitination, Muscle atrophy and Cytosol. His Ubiquitin study which covers Bortezomib that intersects with NFE2L1, MG132 and Unfolded protein response. His study in Protein degradation is interdisciplinary in nature, drawing from both Molecular biology, Activator, Skeletal muscle, Cell cycle and Proteostasis.

Between 2008 and 2020, his most popular works were:

  • Reversal of Cancer Cachexia and Muscle Wasting by ActRIIB Antagonism Leads to Prolonged Survival (656 citations)
  • Muscle wasting in disease: molecular mechanisms and promising therapies (476 citations)
  • During muscle atrophy, thick, but not thin, filament components are degraded by MuRF1-dependent ubiquitylation (454 citations)

In his most recent research, the most cited papers focused on:

  • Enzyme
  • Gene
  • Amino acid

Alfred L. Goldberg mainly investigates Proteasome, Biochemistry, Ubiquitin, Cell biology and Protein degradation. His work focuses on many connections between Proteasome and other disciplines, such as Bortezomib, that overlap with his field of interest in Drug discovery, Pharmacology, Drug development and MG132. His Ubiquitin research includes elements of ATP hydrolysis, Plasma protein binding and Proteolysis.

The various areas that Alfred L. Goldberg examines in his Cell biology study include Proteasome Binding and In vivo. His study looks at the relationship between Protein degradation and fields such as Autophagy, as well as how they intersect with chemical problems. His Ubiquitin ligase research incorporates elements of Endocrinology, Myofibril, Internal medicine, Muscle atrophy and Endosome.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

Inhibitors of the proteasome block the degradation of most cell proteins and the generation of peptides presented on MHC class I molecules

Kenneth L. Rock;Colette Gramm;Lisa Rothstein;Karen Clark.
Cell (1994)

3694 Citations

Structure and Functions of the 20S and 26S Proteasomes

Olivier Coux;Keiji Tanaka;Alfred L. Goldberg.
Annual Review of Biochemistry (1996)

2964 Citations

Foxo Transcription Factors Induce the Atrophy-Related Ubiquitin Ligase Atrogin-1 and Cause Skeletal Muscle Atrophy

Marco Sandri;Claudia Sandri;Alex Gilbert;Carsten Skurk.
Cell (2004)

2791 Citations

Protein degradation and protection against misfolded or damaged proteins

Alfred L. Goldberg.
Nature (2003)

2740 Citations

The ubiquitinproteasome pathway is required for processing the NF-κB1 precursor protein and the activation of NF-κB

Vito J. Palombella;Oliver J. Rando;Alfred L. Goldberg;Tom Maniatis.
Cell (1994)

2682 Citations

Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Daniel J. Klionsky;Hagai Abeliovich;Patrizia Agostinis;Devendra K. Agrawal.
Autophagy (2008)

2530 Citations

Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy

Marcelo D. Gomes;Stewart H. Lecker;R. Thomas Jagoe;Ami Navon.
Proceedings of the National Academy of Sciences of the United States of America (2001)

2189 Citations

Proteasome inhibitors: valuable new tools for cell biologists.

Do Hee Lee;Alfred L Goldberg.
Trends in Cell Biology (1998)

2003 Citations

FoxO3 controls autophagy in skeletal muscle in vivo.

Cristina Mammucari;Giulia Milan;Vanina Romanello;Eva Masiero.
Cell Metabolism (2007)

1806 Citations

Multiple types of skeletal muscle atrophy involve a common program of changes in gene expression

Stewart H. Lecker;R. Thomas Jagoe;Alexander Gilbert;Marcelo Gomes.
The FASEB Journal (2004)

1542 Citations

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