- Immune Cell Function and Interaction
- Cancer-related gene regulation
- Epigenetics and DNA Methylation
- Tissue Engineering and Regenerative Medicine
- Mesenchymal stem cell research
- RNA modifications and cancer
- Immune cells in cancer
- Xenotransplantation and immune response
- Immune Response and Inflammation
- CAR-T cell therapy research
- HVDC Systems and Fault Protection
- Cytokine Signaling Pathways and Interactions
- Immunotherapy and Immune Responses
- Organ Transplantation Techniques and Outcomes
Army Medical University
2015-2024
Southwest Hospital
2015
Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences
2009
NK cells can be rapidly activated in response to cytokines during host defense against malignant or viral infection. However, it remains unclear what mechanisms precisely and regulate the expression of a large number genes involved activating cells. In this study, we discovered that NK-cell N6-methyladenosine (m6A) methylation levels were upregulated upon short-term activation repressed tumor microenvironment (TME). Deficiency methyltransferase-like 3 (METTL3) METTL14 moderately influenced...
Allogeneic mesenchymal stem cells (allo-MSCs) have recently garnered increasing interest for their broad clinical therapy applications. Despite this, many studies shown that allo-MSCs are associated with a high rate of graft rejection unless immunosuppressive is administered to control allo-immune responses. Cytotoxic T-lymphocyte-associated protein 4 (CTLA4) co-inhibitory molecule expressed on T mediates the inhibition T-cell function. Here, we investigated osteogenic differentiation...
<div>Abstract<p>NK cells can be rapidly activated in response to cytokines during host defense against malignant or viral infection. However, it remains unclear what mechanisms precisely and regulate the expression of a large number genes involved activating NK cells. In this study, we discovered that NK-cell <i>N</i><sup>6</sup>-methyladenosine (m<sup>6</sup>A) methylation levels were upregulated upon short-term activation repressed tumor...
<p>Supplementary Figure S3</p>
<p>Supplementary Figure S1</p>
<p>Supplementary Figure S1</p>
<p>Supplementary Figure S7</p>
<p>Supplementary Figure S3</p>
<p>Supplementary Figure S5</p>
<p>Supplementary Figure S6</p>
<div>Abstract<p>NK cells can be rapidly activated in response to cytokines during host defense against malignant or viral infection. However, it remains unclear what mechanisms precisely and regulate the expression of a large number genes involved activating NK cells. In this study, we discovered that NK-cell <i>N</i><sup>6</sup>-methyladenosine (m<sup>6</sup>A) methylation levels were upregulated upon short-term activation repressed tumor...
<p>Supplementary Figure S4</p>
<p>Supplementary Figure S2</p>
<p>Supplementary Figure S2</p>
<p>Supplementary Figure S7</p>
<p>Supplementary Figure S6</p>
<p>Supplementary Figure S5</p>
<p>Supplementary Figure S4</p>