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  • PROJ 测试项目

    Ruifang Cao, Shanghai Institute of Nutrition and Health, CAS,2023.04.19

    Description

    wyf test

    OEP004112

  • PROJ ICC WES

    Shaolai Zhou, Fudan University, Zhongshan Hospital,2024.01.31

    Description

    OEP005036

  • PROJ Newly-designed primers for hadal ecosystem

    Yu Zhang, Shanghai Jiaotong University,2020.12.06

    Description

    The hadal microbial community is largely distinct from shallower marine as well as other well investigated ecosystem. We designed newly candidate primers for bacterial and archaeal communities of the hadal trench to show a more realistic picture.

    OEP001350

  • PROJ Genomic data analysis of 80 Yao samples

    Shuhua Xu, Shanghai Institute of Nutrition and Health, CAS,2023.06.07

    Description

    OEP004182

  • PROJ Loss of Setd2 induces systemic inflammation via embryo-derived Kupffer-like cell differentiation to drive malignant transformation

    Yuanliang Zhang, Shanghai Institute of Hematology,2023.12.07

    Description

    SETD2, a specific histone H3 lysine 36 tri-methyltransferase, is recurrently mutated in hematopoietic malignancies. Setd2 deficiency impairs the self-renewal and competitive potential of hematopoietic stem/progenitor cells (HSPCs), while it promotes a myelodysplastic syndrome-like (MDS) transformation. Nevertheless, the precise oncogenic advantages conferred upon HSPCs by Setd2 loss remain inadequately elucidated. Here, we observed that diseased HSPCs, with completely loss of self-renewal capabilities, can differentiate into embryo-derived Kupffer-like cells, characterized by heightened competitive ability, proliferation, and exacerbated inflammatory effects. The Kupffer-like cells sustain persistent systemic inflammation, thereby forcing the malignant transformation process. Notably, macrophage depletion effectively ameliorates the inflammatory state and alleviates MDS-like symptoms. Mechanistically, loss of Setd2 induces substantial alterations in DNA methylation patterns and chromatin accessibility, which instigate the activation of Irf8 synergistically and/or independently. Consequently, our study posits the notion that the long-lived inflammatory cells differentiated from HSPCs compensate the impaired self-renewal and induce malignant transformation independently.

    OEP004811

  • PROJ 测试项目

    Luo Ruijin, ,2023.11.09

    Description

    武汉开发部分-测试提交

    OEP004707

  • PROJ OEP004177

    Boya Zhang, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine,2023.06.02

    Description

    OEP004177

  • PROJ OEP004193

    Boya Zhang, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine,2023.06.15

    Description

    OEP004193

  • PROJ Intermediate cell population depends on JAK/STAT signaling in prostate basal cell fates determination

    Lin Li, Shanghai Institutes for Biological Sciences,2023.03.09

    Description

    Many glandular epithelia, such as the prostate gland, consist of basal and luminal cells maintained by unipotent stem cells that can revert to multipotency during inflammation or cancer context. However, the defined basal stem cell populations responsible for prostate regeneration and their cell fates in prostate homeostasis, inflammation and carcinogenesis remain unclear. Using a genetic proliferation tracer (ProTracer) system, we found that basal cells exhibited extensive cell turnover during androgen-mediated prostate regression and regeneration. A rare intermediate basal cell population with luminal marker-expressing (termed Basal-B) and a large basal cell population (termed Basal-A) were identified in mouse prostates. Basal-B cells exhibited a greater capacity for organoid formation and luminal cell differentiation in vitro. Genetic lineage tracing showed that Basal-B cell maintained Basal-B cell identity and differentiated to Basal-A cell during androgen-mediated prostate regeneration. Specifically, Basal-B cells showed activation of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway. Inhibiting JAK/STAT signaling markedly reduced the proportion of Basal-B cells in normal mouse prostates. Fate-mapping results showed that Basal-B cells had a greater tendency to generate luminal cells during prostate inflammation. Whereas, JAK/STAT signaling inhibition notably attenuated the efficiency of basal-to-luminal differentiation of Basal-B cells during prostate inflammation. Additionally, deleting the Pten gene in basal cells significantly increased the Nkx3.1-expressing Basal-B like cell population and led to prostatic intraepithelial neoplasia. In humans, Basal-B cells were significantly more prevalent in benign prostate hyperplasia than in normal samples. Our findings identify Basal-B cells as a potential stem cell population and highlight JAK/STAT signaling as a key regulator in determining the cell fates of prostate intermediate Basal-B cells under both physiological and pathological conditions.

    OEP003997

  • PROJ Anaerobic hydrocarbon biodegradation by alkylotrophic methanogens in deep oil reservoirs

    Zhuo Zhou, Biogas Institute of Ministry of Agriculture and Rural Affairs,2023.02.22

    Description

    OEP003873