Jin Hua Liang
A5101477518- Cancer Immunotherapy and Biomarkers
- Immune Cell Function and Interaction
- Immunotherapy and Immune Responses
- SARS-CoV-2 and COVID-19 Research
- CAR-T cell therapy research
- Cytomegalovirus and herpesvirus research
- interferon and immune responses
- Immune responses and vaccinations
- Immune cells in cancer
- Viral-associated cancers and disorders
- HIV Research and Treatment
- Drug-Induced Adverse Reactions
- Immunodeficiency and Autoimmune Disorders
- Ferroptosis and cancer prognosis
- COVID-19 Clinical Research Studies
- Acute Lymphoblastic Leukemia research
- Monoclonal and Polyclonal Antibodies Research
- Neonatal Health and Biochemistry
- Mosquito-borne diseases and control
- Cancer Cells and Metastasis
- Chemokine receptors and signaling
- Medicinal Plant Pharmacodynamics Research
- Natural product bioactivities and synthesis
- Heme Oxygenase-1 and Carbon Monoxide
- Cell Adhesion Molecules Research
Shaanxi University of Chinese Medicine
2023
Broad Institute
2021-2022
Brigham and Women's Hospital
2021-2022
Chinese People's Armed Police Force
2022
Harvard University
2021
Immune checkpoint blockade (ICB) therapy revolutionized cancer treatment, but many patients with impaired MHC-I expression remain refractory. Here, we combined FACS-based genome-wide CRISPR screens a data-mining approach to identify drugs that can upregulate without inducing PD-L1. screening identified TRAF3, suppressor of the NFκB pathway, as negative regulator not The Traf3-knockout gene signature is associated better survival in ICB-naïve and ICB response. We then screened for similar...
Abstract The recently identified Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the cause of COVID-19 pandemic. How this novel beta-coronavirus virus, and coronaviruses more generally, alter cellular metabolism to support massive production ~30 kB viral genomes subgenomic RNAs remains largely unknown. To gain insights, transcriptional metabolomic analyses are performed 8 hours after SARS-CoV-2 infection, an early timepoint where lifecycle completed but prior overt effects on...
We have previously shown that non-cytotoxic concentrations (600-1200 U/ml) of recombinant mouse tumour necrosis factor-alpha (TNF-alpha) can induce differentiation a subclone (JCS) the WEHI-3B myelomonocytic leukaemia cell line into mature cells with characteristics macrophages. In present study, effects interleukin-4 (IL-4), either alone or in combination TNF-alpha, on growth and JCS were examined. IL-4 (20-5000 inhibited dose-dependent manner but did not differentiation. However,...
Serum total bilirubin (STB) is recently more regarded as an antioxidant with vascular protective effects. However, we noticed that elevated STB appeared in unstable angina pectoris (UAP) patients diffused coronary lesions. We aimed to explore STB's roles UAP patients, which have not been reported by articles. 1120 were retrospectively screened, and 296 finally enrolled. They grouped Canadian Cardiovascular Society (CCS) grades. The synergy between PCI TAXUS stent cardiac surgery score...
Chemotherapy is one of the important adjuvant methods for treatment glioblastoma (GBM), and chemotherapy resistance a clinical problem that neurooncologists need to solve urgently. It reported Saikosaponin D (SSD), an active component Bupleurum chinense, had various antitumor activities could also enhance chemosensitivity liver cancer other tumors. However, it not clear whether has effect on glioma its specific mechanism.The CCK8 assay, Wound healing assay Matrigel invasion were used detect...
Summary Epstein-Barr virus (EBV) subverts host epigenetic pathways to switch between viral latency programs, colonize the B-cell compartment and reactivate. Within memory B-cells, reservoir for lifelong infection, EBV genomic DNA histone methylation marks restrict gene expression. But, this strategy also enables EBV-infected tumors, including Burkitt lymphomas evade immune detection. Little is known about cell metabolic that support epigenome landscapes. We therefore used amino acid...
<div>Abstract<p>Immune checkpoint blockade (ICB) therapy revolutionized cancer treatment, but many patients with impaired MHC-I expression remain refractory. Here, we combined FACS-based genome-wide CRISPR screens a data-mining approach to identify drugs that can upregulate without inducing PD-L1. screening identified TRAF3, suppressor of the NFκB pathway, as negative regulator not The <i>Traf3</i>-knockout gene signature is associated better survival in ICB-naïve and...
<div>Abstract<p>Immune checkpoint blockade (ICB) therapy revolutionized cancer treatment, but many patients with impaired MHC-I expression remain refractory. Here, we combined FACS-based genome-wide CRISPR screens a data-mining approach to identify drugs that can upregulate without inducing PD-L1. screening identified TRAF3, suppressor of the NFκB pathway, as negative regulator not The <i>Traf3</i>-knockout gene signature is associated better survival in ICB-naïve and...
<p>RNA-seq and ATAC-seq of TRAF3-normal -deficient B16F10 cells treated with vehicle control or IFNγ</p>
<p>Supplementary Figures S1-S8</p>
<p>Supplementary Figures S1-S8</p>
<p>RNA-seq and ATAC-seq of TRAF3-normal -deficient B16F10 cells treated with vehicle control or IFNγ</p>
<p>Effect of different drug treatment on the expression genes encoding MHC-I, TAP1, PD-L1, and PD-L2</p>
<p>RNA-seq and H3K27ac ChIP-seq of MHC-I-high MHC-I-low primary melanoma samples</p>
<p>Traf3-knockout signature derived from RNA-seq</p>
<p>MAGeCK analysis of CRISPR screen results to identify the regulators MHC-I/PD-L1</p>
<p>Information on the ICB treatment clinical cohorts used in this study</p>
<p>Traf3-knockout signature derived from RNA-seq</p>
<p>RNA-seq and H3K27ac ChIP-seq of MHC-I-high MHC-I-low primary melanoma samples</p>
<p>Information on the ICB treatment clinical cohorts used in this study</p>
<p>MAGeCK analysis of CRISPR screen results to identify the regulators MHC-I/PD-L1</p>
<p>RNA-seq of bulk B16F10 tumors that underwent different treatments</p>
<p>Effect of different drug treatment on the expression genes encoding MHC-I, TAP1, PD-L1, and PD-L2</p>