World's Best Scientists 2026 revealed!

D-Index & Metrics

Biology and Biochemistry

D-Index
67
Citations
12098
World Ranking
8400
National Ranking
3781

Overview

Wei-Ya Ma is affiliated with the University of Minnesota in the United States. Their research spans multiple fields with a primary focus on medicine and biochemistry, genetics, and molecular biology. Subfields that characterize their work include molecular biology, pharmacology, pediatrics, perinatology, child health, speech, hearing, and organic chemistry.

Wei-Ya Ma has contributed to several topics within biomedical research, including:

  • Cannabis and Cannabinoid Research
  • Prenatal Substance Exposure Effects
  • Chemical Synthesis and Analysis
  • Neuroscience of respiration and sleep
  • Receptor Mechanisms and Signaling
  • Inflammatory mediators and NSAID effects
  • Adolescent and Pediatric Healthcare

Their publication record includes papers in multiple scientific journals notable for various research areas. Frequent publication venues include:

  • Journal of Medicinal Chemistry
  • Cancer Research
  • Zenodo (CERN European Organization for Nuclear Research)
  • Progress in Neuro-Psychopharmacology and Biological Psychiatry
  • Journal of Biological Chemistry

Recent papers authored or co-authored by Wei-Ya Ma encompass the following works:

  • "Evaluation of Amide Bioisosteres Leading to 1,2,3-Triazole Containing Compounds as GPR88 Agonists: Design, Synthesis, and Structure-Activity Relationship Studies" (2021, Journal of Medicinal Chemistry)
  • "Investigating the 'two-hit hypothesis': Effects of prenatal maternal immune activation and adolescent cannabis use on neurodevelopment in mice" (2022, Progress in Neuro-Psychopharmacology and Biological Psychiatry)
  • "Structural basis for multifunctional roles of human Ints3 C-terminal domain" (2020, Journal of Biological Chemistry)
  • "Crystal structure of the human PRPK-TPRKB complex" (2021, Communications Biology)
  • "Chronic generalized pain disrupts whole brain functional connectivity in mice" (2021, Brain Imaging and Behavior)

Wei-Ya Ma collaborates frequently with other researchers, indicating active engagement in multidisciplinary studies. Notable co-authors with multiple joint publications include:

  • Emmanuel Darcq
  • Brigitte L. Kieffer
  • Elisa Guma
  • Lani Cupo
  • Daniel Gallino

The combination of Wei-Ya Ma's work covers both fundamental molecular investigations and applied biomedical topics, notably linking substance exposure during prenatal and adolescent stages to neurodevelopmental outcomes. The focus on receptor mechanisms and chemical synthesis complements investigations into pediatric healthcare and inflammatory processes.

Best Publications

  • Resveratrol-induced activation of p53 and apoptosis is mediated by extracellular-signal-regulated protein kinases and p38 kinase.

    Qing Bai She;Ann M. Bode;Wei-Ya Ma;Nan Yue Chen

  • Resveratrol suppresses cell transformation and induces apoptosis through a p53-dependent pathway.

    Chuanshu Huang;Wei-ya Ma;Angela Goranson;Zigang Dong

  • Cell Apoptosis: Requirement of H2AX in DNA Ladder Formation, but Not for the Activation of Caspase-3

    Chengrong Lu;Feng Zhu;Yong Yeon Cho;Faqing Tang

  • p38 Kinase Mediates UV-induced Phosphorylation of p53 Protein at Serine 389

    Chuanshu Huang;Wei Ya Ma;Aaron Maxiner;Yi Sun

  • Suppression of Skin Tumorigenesis in c-Jun NH2-Terminal Kinase-2-Deficient Mice

    Nanyue Chen;Masaaki Nomura;Qing Bai She;Wei-Ya Ma

  • Blocking activator protein-1 activity, but not activating retinoic acid response element, is required for the antitumor promotion effect of retinoic acid

    Chuanshu Huang;Wei-Ya Ma;Marcia I. Dawson;Mercedes Rincon

  • Inhibition of Epidermal Growth Factor-induced Cell Transformation and Activator Protein 1 Activation by [6]-Gingerol

    Ann M. Bode;Wei-Ya Ma;Young Joon Surh;Zigang Dong

  • Arsenic induces apoptosis through a c-Jun NH2-terminal kinase-dependent, p53-independent pathway.

    Chuanshu Huang;Wei-ya Ma;Jingxia Li;Zigang Dong

  • Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced NF-κB activation by tea polyphenols, (–)-epigallocatechin gallate and theaflavins

    Masaaki Nomura;Wei-ya Ma;Nanyue Chen;Ann M. Bode

  • Inhibition of Activator Protein 1 Activity and Neoplastic Transformation by Aspirin

    Zigang Dong;Chuanshu Huang;Rhoderick E. Brown;Wei Ya Ma

  • Resveratrol directly targets COX-2 to inhibit carcinogenesis†

    Tatyana A Zykova;Feng Zhu;Xiuhong Zhai;Wei-Ya Ma

  • Calcium-activated RAF/MEK/ERK Signaling Pathway Mediates p53-dependent Apoptosis and Is Abrogated by αB-Crystallin through Inhibition of RAS Activation

    David Wan Cheng Li;Jin Ping Liu;Ying Wei Mao;Ying Wei Mao;Hua Xiang

  • Two novel glycosides from the fruits of Morinda citrifolia (noni) inhibit AP-1 transactivation and cell transformation in the mouse epidermal JB6 cell line.

    Guangming Liu;Ann Bode;Wei-Ya Ma;Shengmin Sang

  • Shortage of mitogen-activated protein kinase is responsible for resistance to AP-1 transactivation and transformation in mouse JB6 cells

    Chuanshu Huang;Wei-Ya Ma;Matthew R. Young;Nancy Colburn

  • Requirement of Erk, but not JNK, for arsenite-induced cell transformation.

    Chuanshu Huang;Wei-Ya Ma;Jingxia Li;Angela Goranson

  • Requirement for phosphatidylinositol 3-kinase in epidermal growth factor-induced AP-1 transactivation and transformation in JB6 P+ cells.

    Chuanshu Huang;Wei Ya Ma;Zigang Dong

  • Induction of Apoptosis by Caffeine Is Mediated by the p53, Bax, and Caspase 3 Pathways

    Zhiwei He;Wei Ya Ma;Takashi Hashimoto;Ann M. Bode

  • Inhibition of Ultraviolet B-induced Activator Protein-1 (AP-1) Activity by Aspirin in AP-1-Luciferase Transgenic Mice

    Chuanshu Huang;Wei-Ya Ma;David Hanenberger;Margot P. Cleary

  • Translocation of Protein Kinase Cε and Protein Kinase Cδ to Membrane Is Required for Ultraviolet B-induced Activation of Mitogen-activated Protein Kinases and Apoptosis *

    Nanyue Chen;Wei-ya Ma;Chuanshu Huang;Zigang Dong

  • Involvement of the acid sphingomyelinase pathway in uva-induced apoptosis.

    Yiguo Zhang;Peter Mattjus;Patricia C. Schmid;Ziming Dong

Frequent Co-Authors

Zigang Dong
Zigang Dong University of Minnesota
Ann M. Bode
Ann M. Bode University of Minnesota
Chuanshu Huang
Chuanshu Huang New York University
Feng Zhu
Feng Zhu Zhejiang University
Chung S. Yang
Chung S. Yang Rutgers, The State University of New Jersey
Jingxia Li
Jingxia Li New York University
G. Tim Bowden
G. Tim Bowden University of Arizona
Chi-Tang Ho
Chi-Tang Ho Rutgers, The State University of New Jersey
Min Ding
Min Ding National Institute for Occupational Safety and Health
Rhoderick E. Brown
Rhoderick E. Brown University of Minnesota

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