Project description:Protein arginine methylation is an important process, which regulates diverse cellular functions including cell proliferation, RNA stability, DNA repair and gene transcription. Based on literature search, protein arginine methyltransferase (PRMT) indeed plays important roles in colon cancer pathophysiology. The PRMT expression level is involved in colon cancer patient’s survival and has been suggested to be a prognostic marker in colon cancer patients. Recently, our group found a novel methylation on epidermal growth factor receptor (EGFR), which affected EGFR downstream signaling. investigators further observed the methylation event on EGFR not only regulated tumor growth in mouse xenograft model but also influenced cetuximab response in colon cancer cell lines. To further study the clinical correlation between EGFR methylation and cetuximab response, we propose to detect EGFR methylation level in paraffin embedded tissue samples from colorectal cancer patients with or without cetuximab treatment by IHC staining and analyze its correlation with cetuximab response. This study will provide an insight to the strategy of colorectal cancer therapy.
Project description:<p>High-throughput linking of T cell receptor (TCR) sequences to their binding antigens is vital for immune profiling, yet challenging. We present Tetramer associated TCR Sequencing (TetTCR-Seq) to address this challenge. Binding is determined using a library of DNA-barcoded antigen tetramers that are rapidly and inexpensively generated using an in vitro transcription/translation platform. We included CMV+ donors (CMV seropositive donors who are infected with Cytomegalovirus) to screen for CMV specific TCRs.</p>
Project description:Previous articles have reported that mouse cell lines infected with hepatitis virus do not produce interferon, which only causes natural immune responses when infected with macrophages and dendritic cells. Therefore, we collected the cells of MHV-infected mouse dendritic cells for 18 hours, and detected the immune-related factors and other altered genes in the cells after infection by Proteomics analysis
Project description:Transcription profiling by array of mouse male retinas to investigate IGF-I-induced chronic gliosis and retinal stress IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with the increased production of pro-inflammatory cytokines, potential mediators of neuronal death.
Project description:Transcription profiling by array of mouse male retinas to investigate IGF-I-induced chronic gliosis and retinal stress IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with the increased production of pro-inflammatory cytokines, potential mediators of neuronal death. 3 transgenic and 3 wild type biological replicates examined.