A5026304917- Sirtuins and Resveratrol in Medicine
- RNA regulation and disease
- RNA modifications and cancer
- Autophagy in Disease and Therapy
- Cytomegalovirus and herpesvirus research
- Endoplasmic Reticulum Stress and Disease
- Cancer-related molecular mechanisms research
- Adenosine and Purinergic Signaling
- Dermatologic Treatments and Research
- Prostate Cancer Treatment and Research
- Skin Protection and Aging
- Lymphoma Diagnosis and Treatment
- Lysosomal Storage Disorders Research
- Monoclonal and Polyclonal Antibodies Research
- Folate and B Vitamins Research
- Stress Responses and Cortisol
- HER2/EGFR in Cancer Research
- Adipose Tissue and Metabolism
- Glutathione Transferases and Polymorphisms
- Epigenetics and DNA Methylation
- Angiogenesis and VEGF in Cancer
- Pharmacological Effects and Assays
- Biochemical and Molecular Research
- Immune Cell Function and Interaction
- Radiopharmaceutical Chemistry and Applications
Beijing Normal University
2024
Indiana University School of Medicine
2011
Indiana University – Purdue University Indianapolis
2011
Aarhus University Hospital
2008
Follicular helper T (TFH) cells are essential for inducing germinal center (GC) reactions to mediate humoral adaptive immunity in tumors; however, the mechanisms underlying TFH-cell differentiation remain unclear. In this study, we found that metabolism sensor sirtuin 3 (SIRT3) is critical and GC formation during tumor development viral infection. SIRT3 deficiency CD4+ intrinsically enhanced Mechanistically, damaged oxidative phosphorylation (OXPHOS) compensatively triggered NAD+-glycolysis...
Studies have consistently shown that long-wave ultraviolet A (UVA) radiation triggers skin photoaging, which is evident as reduced elasticity, a loss of firmness, and signs aging. There an urgent need to investigate photoaging mechanisms devise protective strategies against UVA. The present study aimed explore the effects recombinant type XVII collagen on UVA-induced aging uncover its molecular mechanisms, thereby laying solid theoretical foundation for precise treatments prevention. We...
Abstract Anti-CTLA-4 antibody is considered the “forefront” of immune checkpoint inhibitors as it plays a critical role in preventing CTLA-4 mediated inhibitory signals that downregulate T-cell responses, and functioning early at initial phase naive activation. However, not tumor associated antigen it’s expressed variety normal tissues such lymph nodes, tonsil lung, therefore anti-CTLA-4 can trigger severe on-target, off-tumor toxicities immune-related adverse events (irAEs), substantially...
Associations of P16, MGMT, hMLH1 and hMLH2 with gastric cancer their relation MTHFR status in patients who were confirmed pathological diagnosis assessed. Aberrant DNA methylation polymorphisms C677T assayed. The proportional hypermethylation tissues was significantly higher than remote normal-appearing tissues. P16 MGMT correlated the T N stages. Individuals homozygotes (TT) had significant risk [OR (95% CI)= 3.47(1.41-7.93)]. However, we did not find association between polymorphism genes...
<div>Abstract<p>Follicular helper T (T<sub>FH</sub>) cells are essential for inducing germinal center (GC) reactions to mediate humoral adaptive immunity in tumors; however, the mechanisms underlying T<sub>FH</sub>-cell differentiation remain unclear. In this study, we found that metabolism sensor sirtuin 3 (SIRT3) is critical and GC formation during tumor development viral infection. SIRT3 deficiency CD4<sup>+</sup> intrinsically enhanced...
<p>Fig.S10. SIRT3 is required for promoting T<sub>FH</sub> differentiation and GC responses <i>in vivo</i>.</p>
<p>Fig.S19. SIRT3 deficiency promotes T<sub>FH</sub> differentiation through mTOR and NAD<sup>+</sup> pathway.</p>
<p>Fig.S14. Oxidative phosphorylation is required for T<sub>FH</sub> differentiation induced by <i>Sirt3</i><sup><i>∆CD4</i></sup>.</p>
<p>Fig.S11. SIRT3 negatively affects efficient GC responses after immunization via antigen-specific mechanisms.</p>
<p>Fig. S15. SIRT3 deficiency upregulates the expression of Glut1 and p-S6 in T<sub>FH</sub> cells tumor.</p>
<p>Fig. S13. NAD<sup>+</sup> levels are crucial for T<sub>FH</sub> cell differentiation induced by <i>Sirt3</i><sup><i>∆CD4</i></sup> in tumor.</p>
<p>Fig. S18. SIRT3 deficiency promotes T<sub>FH</sub> differentiation through mTOR-HIF1α coupled with NAD<sup>+</sup>-dependent glucose metabolism pathway.</p>
<p>Fig. S16. SIRT3 deficiency upregulates the expressions of HIF1α</p>
<p>Fig.S12. SIRT3 deficiency enhances T<sub>FH</sub> cell differentiation <i>in vitro</i>.</p>
<p>Fig.S17. SIRT3 deficiency promotes T<sub>FH</sub> cell differentiation through mTOR-HIF1α coupled with the NAD<sup>+</sup>-dependent glucose metabolism pathway in mice.</p>
<div>Abstract<p>Follicular helper T (T<sub>FH</sub>) cells are essential for inducing germinal center (GC) reactions to mediate humoral adaptive immunity in tumors; however, the mechanisms underlying T<sub>FH</sub>-cell differentiation remain unclear. In this study, we found that metabolism sensor sirtuin 3 (SIRT3) is critical and GC formation during tumor development viral infection. SIRT3 deficiency CD4<sup>+</sup> intrinsically enhanced...
<p>Fig.S11. SIRT3 negatively affects efficient GC responses after immunization via antigen-specific mechanisms.</p>
<p>Fig. S13. NAD<sup>+</sup> levels are crucial for T<sub>FH</sub> cell differentiation induced by <i>Sirt3</i><sup><i>∆CD4</i></sup> in tumor.</p>
<p>Fig. S1. SIRT3 expression is related to the TFH differentiation in viral infection and cancer.</p>
<p>Fig.S12. SIRT3 deficiency enhances T<sub>FH</sub> cell differentiation <i>in vitro</i>.</p>
<p>Fig. S1. SIRT3 expression is related to the TFH differentiation in viral infection and cancer.</p>
<p>Fig.S10. SIRT3 is required for promoting T<sub>FH</sub> differentiation and GC responses <i>in vivo</i>.</p>
<p>Fig.S14. Oxidative phosphorylation is required for T<sub>FH</sub> differentiation induced by <i>Sirt3</i><sup><i>∆CD4</i></sup>.</p>
<p>Fig. S15. SIRT3 deficiency upregulates the expression of Glut1 and p-S6 in T<sub>FH</sub> cells tumor.</p>