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Biology and Biochemistry

D-Index
118
Citations
69673
World Ranking
689
National Ranking
435

Overview

Albert S. Baldwin is affiliated with the University of North Carolina at Chapel Hill in the United States. Their research contributions span across biochemistry, genetics, molecular biology, and medicine, with particular emphasis on molecular biology, cancer research, immunology, oncology, and genetics.

The scientist's main research focus includes:

  • NF-κB Signaling Pathways
  • Epigenetics and DNA Methylation
  • Interferon and Immune Responses
  • Cytokine Signaling Pathways and Interactions
  • Immune Response and Inflammation
  • Cancer, Hypoxia, and Metabolism
  • CAR-T Cell Therapy Research

Albert S. Baldwin has produced a significant body of work, with 141 publications in the broader areas of biochemistry, genetics, and molecular biology, and 69 publications in medicine. Their work has been published mainly in the following venues:

  • UNC Libraries
  • Neuro-Oncology
  • Proceedings of the National Academy of Sciences
  • bioRxiv (Cold Spring Harbor Laboratory)
  • The Journal of Immunology

Recent notable papers authored or co-authored by Baldwin include:

  • "Itaconate inhibits TET DNA dioxygenases to dampen inflammatory responses," 2022, Nature Cell Biology
  • "Expanding the View of IKK: New Substrates and New Biology," 2021, Trends in Cell Biology
  • "Genome-wide Screening Identifies SFMBT1 as an Oncogenic Driver in Cancer with VHL Loss," 2020, Molecular Cell
  • "USP37 promotes deubiquitination of HIF2α in kidney cancer," 2020, Proceedings of the National Academy of Sciences
  • "USP13 promotes deubiquitination of ZHX2 and tumorigenesis in kidney cancer," 2022, Proceedings of the National Academy of Sciences

Frequent collaborators in their research include Shawn Hingtgen, Jeremy M. Simon, Rajaneekar Dasari, Andrew Satterlee, and Krishna Kanchi, each having co-authored multiple publications with Baldwin. These collaborations contribute to a body of work characterized by cross-disciplinary inquiry into molecular mechanisms of disease and immune signaling.

Best Publications

  • THE NF-κB AND IκB PROTEINS: New Discoveries and Insights

    Albert S. Baldwin

  • NF-κB Antiapoptosis: Induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to Suppress Caspase-8 Activation

    Cun Yu Wang;Marty W. Mayo;Robert G. Korneluk;David V. Goeddel

  • TNF- and Cancer Therapy-Induced Apoptosis: Potentiation by Inhibition of NF-κB

    Cun Yu Wang;Marty W. Mayo;Albert S Baldwin

  • Role of Transcriptional Activation of IκBα in Mediation of Immunosuppression by Glucocorticoids

    Robert I. Scheinman;Patricia C. Cogswell;Alan K. Lofquist;Albert S. Baldwin

  • Control of oncogenesis and cancer therapy resistance by the transcription factor NF-κB

    Albert S. Baldwin

  • NF-κB Controls Cell Growth and Differentiation through Transcriptional Regulation of Cyclin D1

    Denis C. Guttridge;Chris Albanese;Julie Y. Reuther;Richard G. Pestell

  • Series Introduction: The transcription factor NF-κB and human disease

    Albert S. Baldwin

  • Control of inducible chemoresistance: Enhanced anti-tumor therapy through increased apoptosis by inhibition of NF-κB

    Cun Yu Wang;James C. Cusack;Rong Liu;Albert S. Baldwin

  • Tumor necrosis factor and interleukin-1 lead to phosphorylation and loss of I kappa B alpha: a mechanism for NF-kappa B activation.

    A A Beg;T S Finco;P V Nantermet;A S Baldwin

  • Characterization of mechanisms involved in transrepression of NF-kappa B by activated glucocorticoid receptors.

    R I Scheinman;A Gualberto;C M Jewell;J A Cidlowski

  • The I kappa B proteins: multifunctional regulators of Rel/NF-kappa B transcription factors.

    Amer A. Beg;Albert S. Baldwin

  • NF-κB-Induced Loss of MyoD Messenger RNA: Possible Role in Muscle Decay and Cachexia

    Denis C. Guttridge;Marty W. Mayo;Lee V. Madrid;Cun-Yu Wang

  • I kappa B interacts with the nuclear localization sequences of the subunits of NF-kappa B: a mechanism for cytoplasmic retention.

    A. A. Beg;S. M. Ruben;R. I. Scheinman;S. Haskill

  • Akt Stimulates the Transactivation Potential of the RelA/p65 Subunit of NF-κB through Utilization of the IκB Kinase and Activation of the Mitogen-activated Protein Kinase p38

    Lee V. Madrid;Marty W. Mayo;Julie Y. Reuther;Albert S. Baldwin

  • Phase I Trial of the Proteasome Inhibitor PS-341 in Patients With Refractory Hematologic Malignancies

    Robert Z. Orlowski;Thomas E. Stinchcombe;Beverly S. Mitchell;Thomas C. Shea

  • Characterization of an immediate-early gene induced in adherent monocytes that encodes IκB-like activity

    Stephen Haskill;Amer A. Beg;S.Mark Tompkins;John S. Morris

  • The p65 (RelA) Subunit of NF-κB Interacts with the Histone Deacetylase (HDAC) Corepressors HDAC1 and HDAC2 To Negatively Regulate Gene Expression

    Brian P. Ashburner;Sandy D. Westerheide;Albert S. Baldwin

  • Cross-coupling of the NF-kappa B p65 and Fos/Jun transcription factors produces potentiated biological function.

    Bernd Stein;Albert S. Baldwin;Dean W. Ballard;Warner C. Greene

  • Nuclear factor-kappaB and inhibitor of kappaB kinase pathways in oncogenic initiation and progression.

    D S Bassères;A S Baldwin

  • Akt suppresses apoptosis by stimulating the transactivation potential of the RelA/p65 subunit of NF-κB

    Lee V. Madrid;Cun Yu Wang;Denis C. Guttridge;Arndt J G Schottelius

Frequent Co-Authors

Amer A. Beg
Amer A. Beg University of South Florida
Denis C. Guttridge
Denis C. Guttridge Medical University of South Carolina
Qing Zhang
Qing Zhang Nanyang Technological University
Jonathan S. Serody
Jonathan S. Serody University of North Carolina at Chapel Hill
Roland Tisch
Roland Tisch University of North Carolina at Chapel Hill
Cun-Yu Wang
Cun-Yu Wang University of California, Los Angeles
Devanand Sarkar
Devanand Sarkar Virginia Commonwealth University
Paul B. Fisher
Paul B. Fisher Virginia Commonwealth University
Charles M. Perou
Charles M. Perou University of North Carolina at Chapel Hill
Jenny P.-Y. Ting
Jenny P.-Y. Ting University of North Carolina at Chapel Hill

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