Transcriptional Regulation and Chromatin Structure Research: Investigate the role of CHR5 in maintaining chromatin structure and regulating the initiation and elongation of gene transcription. Evaluate the impact of CHR5 deficiency on the global transcriptome and epigenetic landscape. Stem Cell Self-Renewal and Differentiation Research: Explore the regulatory functions of CHR5 in the self-renewal, pluripotency maintenance, and lineage-specific differentiation of embryonic stem cells or pluripotent stem cells. Study the effects of CHR5 deletion on stem cell differentiation potential and tissue-specific gene expression programs. Embryonic Development and Organogenesis Research: Investigate the critical role of CHR5 in early embryonic development, trilaminar differentiation, and organ formation. Assess developmental defects, growth abnormalities, and potential lethal phenotypes resulting from CHR5 deficiency. Cancer Initiation and Progression Research: Study the role of CHR5 in tumorigenesis, cell cycle regulation, DNA damage response, and metastasis. Evaluate the feasibility of targeting CHR5 for cancer therapy and its associated signaling pathways.

1. Research on tumor suppression and epigenetic regulation: Investigate the effect of USP7 ubiquitination enzyme deficiency on the stability of key tumor suppressor proteins (such as p53, PTEN) and epigenetic regulatory factors (such as EZH2, DNMT1), and elucidate its mechanism of action in tumor occurrence, development, and treatment resistance. Evaluate the potential efficacy of small molecule inhibitors targeting USP7 in tumor therapy. 2. Neurodevelopment and neurodegenerative diseases: Study the role of USP7 in neuron development, synaptic function, and survival, and explore its potential association with neurodevelopmental disorders (such as autism spectrum disorders) or neurodegenerative diseases (such as Alzheimer's disease). 3. Immune cell function and autoimmune diseases: Explore the regulatory role of USP7 in the activation, differentiation, and function of immune cells such as T cells and B cells, and assess its function in autoimmune diseases and inflammatory reactions.

1. Research on the mechanism of autoimmune diseases: Explore the regulatory effects of the absence of solute carrier family 15 member 4 (SLC15A4) on Toll-like receptor (TLR) and NOD-like receptor (NLR) signaling pathways (especially TLR7/9 and NOD2 pathways), and its function in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE). Study how SLC15A4-mediated lysosomal amino acid transport affects mTORC1 signaling, autophagy, and inflammasome activation. 2. Natural immune signal transduction: Assess the critical role of SLC15A4 in the production of type I interferons (IFN-α/β) by plasmacytoid dendritic cells (pDC) and pro-inflammatory cytokines (such as TNF-α, IL-6) by myeloid cells. 3. Research on inflammatory bowel disease (IBD): Explore the role of SLC15A4 in maintaining intestinal immune homeostasis and assess its pathological contribution in IBD models (such as Crohn's disease).

1. Research on the fine regulation of apoptosis signaling pathways: Studying the effects of specific Bcl2 point mutations (such as BH3 domain, loop domain mutations) on their anti-apoptotic function, protein interactions (such as with Bax/Bak, BH3-only proteins), and subcellular localization, revealing the precise molecular mechanism by which Bcl2 family proteins regulate cell fate. Exploring the role of Bcl2 gain-of-function or loss-of-function mutations in tumor occurrence, development, and treatment resistance. 2. Tumor Targeted Therapy and Resistance Mechanisms: Simulating tumor resistance caused by Bcl2 mutations in clinical settings, evaluating the efficacy differences of Bcl2 inhibitors (such as Venetoclax/ABT-199) on different mutant variants, guiding personalized treatment strategies. Studying how Bcl2 mutations affect the mitochondrial apoptosis threshold and cross-talk with other apoptosis pathways (such as death receptor pathways). 3. Development and Tissue Homeostasis: Exploring the effects of key Bcl2 point mutations on embryonic development, lymphocyte homeostasis, and the integrity of tissues and organs.

1. Research on RNA modification function and mechanism: Explore the effects of Trmt61a point mutation on the global level and specific distribution of tRNA m1A (N1-methyladenosine) modification, and elucidate its function in translation regulation, cell metabolism, and signal transduction. Study how RNA modification enzyme dysfunction affects cell fate and tissue homeostasis by altering protein synthesis efficiency, abundance, and quality. 2. Exploration of tumor biology and therapeutic targets: Assess the role of Trmt61a gain-of-function or loss-of-function mutations in tumor occurrence, development, metabolic reprogramming, and treatment resistance. Explore the feasibility of targeting the tRNA modification pathway (such as m1A modification) as a new strategy for tumor treatment. 3. Development and stem cell biology: Study the regulatory role of Trmt61a-mediated tRNA modification in embryonic development, tissue and organ formation, and the maintenance of adult stem cell function.

1. Research on the Mechanism of Fibrosis Diseases: Investigate the role of urokinase-type plasminogen activator receptor (uPAR/Plaur) in the process of tissue fibrosis such as pulmonary fibrosis, liver fibrosis, and renal fibrosis. Explore the mechanisms of extracellular matrix degradation, cell migration, and myofibroblast activation mediated by Plaur. 2. Tumor Invasion and Metastasis: Assess the function of Plaur in tumor cell invasion, metastasis, and epithelial-mesenchymal transition (EMT). Study the therapeutic potential of targeting the Plaur or its ligand uPA signaling pathway in inhibiting tumor metastasis. 3. Inflammation and Angiogenesis: Explore the regulatory role of Plaur in inflammation, angiogenesis, and tissue repair.

1. Systemic Lupus Erythematosus (SLE) Mechanism Research: Investigate the impact of HNRNPLL point mutation on RNA splicing regulation and its role in abnormal T cell activation and autoantibody production. Simulate human SLE-related gene mutations to study the molecular and cellular mechanisms of autoimmune reactions caused by HNRNPLL functional abnormality. 2. RNA Splicing and Immune Regulation: Study the mechanism by which HNRNPLL regulates alternative splicing in immune cells (especially T cells), affecting cell surface receptor (such as CD45) expression and function. Assess the impact of HNRNPLL mutations on the development, differentiation, and function of immune cells. 3. Drug Discovery and Targeted Therapy: Provide disease models for the screening and validation of drugs targeting RNA splicing regulation or HNRNPLL-related pathways.

1. Tumor Immunotherapy Evaluation: Research on the role of indoleamine 2,3-dioxygenase 1 (IDO1)-mediated tryptophan metabolism in tumor immune escape. Evaluate the synergistic antitumor effects of IDO1 inhibitors, IDO1 targeted drugs, and combined immunotherapy with immune checkpoint inhibitors (such as anti-PD-1/PD-L1 antibodies). 2. Autoimmune and Inflammatory Diseases: Explore the role of IDO1 in regulating T cell function, inducing immune tolerance, and inhibiting autoimmune reactions. Establish autoimmune disease and chronic inflammatory models related to IDO1 deficiency, and study their pathogenesis. 3. Metabolism and Immune Microenvironment: Assess the impact of IDO1-mediated tryptophan metabolites (such as kynurenine) on tumor microenvironment and immune cell function.

1. Inflammation and Immune Cell Migration Research: Studying the chemotaxis and recruitment mechanisms of monocytes/macrophages to inflammatory sites (such as atherosclerotic plaques, arthritic joints, and neuroinflammatory regions). Exploring the role of the CCR2-CCL2 signaling axis in various acute and chronic inflammatory diseases (such as multiple sclerosis, asthma, pancreatitis). 2. Tumor Immunity and Tumor Microenvironment: Researching the recruitment, polarization, and the role of tumor-associated macrophages (TAMs) in tumor progression, angiogenesis, and immune suppression. Assessing the potential of targeting the CCR2-CCL2 axis in tumor immunotherapy (such as combined immune checkpoint inhibitors, chemotherapy). 3. Metabolism and Cardiovascular Diseases: Investigating the role of CCR2 in metabolic diseases such as obesity, insulin resistance, non-alcoholic fatty liver disease (NAFLD), and atherosclerosis.

1. Research on Virus-Host Interactions: In-depth investigation of the regulatory mechanism of Parp12 in antiviral innate immune responses (such as against coronaviruses, influenza viruses, Zika viruses, etc.). Assess the impact of Parp12 deficiency on viral replication, transmission, and pathogenicity. 2. Tumor Immunology and Treatment: Study the role of Parp12 in tumor development and progression, particularly its function in regulating the tumor microenvironment and immune cell function (such as T cells, macrophages). Evaluate the potential value of targeting the Parp12 signaling pathway in tumor immunotherapy. 3. Inflammation and Autoimmune Diseases: Explore the role of Parp12 in the regulation of inflammatory signaling pathways (such as NF-κB, interferon pathways) and the pathogenesis of autoimmune diseases (such as arthritis, systemic lupus erythematosus).