Demin Wang

ORCID: 0000-0001-5549-3795
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Platelet Disorders and Treatments
  • Cytokine Signaling Pathways and Interactions
  • Heparin-Induced Thrombocytopenia and Thrombosis
  • NF-κB Signaling Pathways
  • Nuclear Structure and Function
  • Cell Adhesion Molecules Research
  • Immune Response and Inflammation
  • Cancer Immunotherapy and Biomarkers
  • Multiple Myeloma Research and Treatments
  • Cell death mechanisms and regulation
  • Immunodeficiency and Autoimmune Disorders
  • interferon and immune responses
  • Immune cells in cancer
  • Acute Myeloid Leukemia Research
  • Protein Kinase Regulation and GTPase Signaling
  • Immunotherapy and Immune Responses
  • Venous Thromboembolism Diagnosis and Management
  • PI3K/AKT/mTOR signaling in cancer
  • CAR-T cell therapy research
  • IL-33, ST2, and ILC Pathways
  • Mast cells and histamine
  • Hematopoietic Stem Cell Transplantation
  • Protein Degradation and Inhibitors

Versiti Blood Center of Wisconsin
2015-2024

Medical College of Wisconsin
2015-2024

Henan University of Technology
2024

Royal United Hospital
2023

Guangdong 999 Brain Hospital
2022

Institute of Process Engineering
2022

Fujian Normal University
2017-2020

Tianjin University of Science and Technology
2016-2017

China International Science and Technology Cooperation
2016-2017

Lanzhou University
2014

Interleukin-17 (IL-17)-producing helper T (TH) cells, named as THIL-17, TH17, or inflammatory TH (THi), have been recently identified a novel effector lineage. However, how cytokine signals mediate THi differentiation is unclear. We found that IL-6 functioned to up-regulate IL-23R and IL-23 synergized with in promoting generation. STAT3, activated by both IL-23, plays critical role development. A hyperactive form of STAT3 promoted development, whereas this process was greatly impaired...

10.1074/jbc.c600321200 article EN cc-by Journal of Biological Chemistry 2007-02-04

The narrow host range of Mycobacterium leprae and the fact that it is refractory to growth in culture has limited research on biologic understanding leprosy. Host genetic factors are thought influence susceptibility infection as well disease progression.We performed a two-stage genomewide association study by genotyping 706 patients 1225 controls using Human610-Quad BeadChip (Illumina). We then tested three independent replication sets for an between presence leprosy 93 single-nucleotide...

10.1056/nejmoa0903753 article EN New England Journal of Medicine 2009-12-18

Many receptor and nonreceptor tyrosine kinases activate phosphoinositide 3-kinases (PI3Ks). To assess the role of delta isoform p110 catalytic subunit PI3Ks, we derived enzyme-deficient mice. The mice are viable but have decreased numbers mature B cells, a block in pro-B-cell differentiation, B1 B-cell deficiency. Both immunoglobulin M receptor-induced Ca(2+) flux proliferation response to mitogens attenuated. Immunoglobulin levels substantially. ability respond T-cell-independent antigens...

10.1128/mcb.22.24.8580-8591.2002 article EN Molecular and Cellular Biology 2002-11-21

AbstractThe cytoplasmic domain of the erythropoietin receptor (EpoR) contains a membrane-distal region that is dispensable for mitogenesis but required recruitment and tyrosine phosphorylation variety signaling proteins. The membrane-proximal 96 amino acids necessary sufficient as well Jak2 activation, induction c-fos, c-myc, cis, T-cell γ locus (TCR-γ), c-pim-1. studies presented here demonstrate this also activation Stat5A Stat5B. single tyrosine, Y-343, which when mutated eliminates...

10.1128/mcb.16.4.1622 article EN Molecular and Cellular Biology 1996-04-01

Stat5 was initially identified as a prolactin-induced member of the signal transducer and activator transcription (Stat) family in sheep. However, is also activated response to variety cytokines. In mice, possibly other species, there exist two genes (Stat5a Stat5b) that encode proteins 92 94 kDa are 95% identical. studies described here, we demonstrate naturally occurring carboxyl-truncated, variant 77 80 these inducibly tyrosine phosphorylated several cytokines form heterodimers with...

10.1128/mcb.16.11.6141 article EN Molecular and Cellular Biology 1996-11-01

Abstract Immune-checkpoint protein V-domain immunoglobulin suppressor of T-cell activation (VISTA) controls antitumor immunity and is a valuable target for cancer immunotherapy. This study identified role VISTA in regulating Toll-like receptor (TLR) signaling myeloid cells controlling cell–mediated inflammation immunosuppression. modulated the polyubiquitination expression TRAF6. Consequently, dampened TLR-mediated MAPK/AP-1 IKK/NF-κB cascades. At cellular levels, regulated effector...

10.1158/2326-6066.cir-18-0489 article EN Cancer Immunology Research 2019-07-24

Control of chronic viral infections by CD8 T cells is critically dependent on CD4 help. In particular, helper-derived IL-21 plays a key role in sustaining the cell response; however, molecular pathways which sustains immunity remain unclear. We demonstrate that causes phenotypic switch transcription factor expression during infection characterized sustained BATF expression. Importantly, both required for optimal persistence and anti-viral effector function sufficient to rescue "unhelped"...

10.1016/j.celrep.2015.09.069 article EN cc-by Cell Reports 2015-11-01

Altered expression of XPO1, the main nuclear export receptor in eukaryotic cells, has been observed cancer, and XPO1 a focus anticancer drug development. However, mechanistic evidence for cancer-specific alterations function is lacking. Here, genomic analysis 42,793 cancers identified recurrent previously unrecognized mutational hotspots XPO1. mutations exhibited striking lineage specificity, with enrichment variety B-cell malignancies, introduction single amino acid substitutions initiated...

10.1158/2159-8290.cd-19-0298 article EN Cancer Discovery 2019-07-08

Abstract Many autoimmune diseases are characterized by the production of autoantibodies. The current view is that CD4 + T follicular helper (Tfh) cells main subset regulating autoreactive B cells. Here we report a CXCR5 PD1 Tfh CD8 whose development and function negatively modulated Stat5. These regulate germinal center cell response control autoantibody production, as deficiency Stat5 in leads to an increase cells, resulting breakdown tolerance concomitant production. share similar gene...

10.1038/s41467-019-12446-5 article EN cc-by Nature Communications 2019-09-27
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