1. Systemic, inducible gene conditional knockout/activation: Hybridized with genetically modified mice carrying Floxed sequences, and induced by tamoxifen, it can achieve time-specific, reversible knockout or activation of the target gene in almost all tissue cell types, used for studying the systemic or specific developmental stage functions of genes in development, physiology, and disease. 2. Systemic lineage tracing and cell fate mapping construction: Hybridized with reporter gene mice (such as Rosa26-LSL-tdTomato), and induced by tamoxifen, it can label almost all cell types and their descendants at the induction time point, used for constructing cell fate maps, tracing cell lineages, and studying tissue regeneration and stem cell differentiation. 3. Gene function study at specific time windows: By controlling the administration time of tamoxifen, gene function can be manipulated at specific time windows during embryonic stage, postnatal, or adulthood, to study the role of genes at different life stages.

1. Specific gene function study of myeloid cells (neutrophils/macrophages): By combining Floxed mouse strains, time- and cell type-specific gene knockout or activation is achieved in lysosome 2 (Lyz2) positive cells (mainly including neutrophils, monocytes, and the majority of tissue macrophages derived from them), for studying the role of specific genes in myeloid cell development, inflammatory response, phagocytosis and杀菌, and tissue repair. 2. Inflammation and infection models: In acute or chronic inflammation and infection models, by tamoxifen induction, the gene function of neutrophils/macrophages is manipulated at specific time points to study their dynamic roles in host defense, inflammation resolution, and immune pathology. 3. Tumor immunology and tumor-associated myeloid cells (TAMs/TANs) research: In the tumor microenvironment, the gene function of tumor-associated macrophages (TAMs) or tumor-associated neutrophils (TANs) is specifically manipulated to assess their impact on tumor progression, angiogenesis, metastasis, and immune treatment response.

1. Research on the specific gene function of macrophages and monocytes: By combining Floxed mouse strains, specific gene knockout or activation is achieved in macrophages, monocytes, and their precursor cells (marked by the colony stimulating factor 1 receptor Csf1r expression) to study the role of specific genes in the development, differentiation, polarization, function (such as phagocytosis, antigen presentation, cytokine secretion), and maintenance of tissue homeostasis of macrophages. 2. Research on tumor immunity and tumor-associated macrophages (TAMs): In the tumor microenvironment, the gene function of TAMs is specifically manipulated to study their critical roles in tumor growth, angiogenesis, immune suppression, and metastasis, and to evaluate targeted TAMs treatment strategies. 3. Inflammation and autoimmune disease models: Constructing myeloid cell-specific gene modification models to study the pathogenic mechanisms of macrophages/monocytes in inflammatory diseases (such as arthritis, atherosclerosis) and autoimmune diseases (such as multiple sclerosis). 4. Research on tissue-resident macrophages: Studying the development, maintenance, and function of resident macrophages in different tissues (such as brain microglia, liver Kupffer cells, alveolar macrophages, peritoneal macrophages, etc.).

1. Research on the Functional Genomics of Intestinal Epithelial Cells: By combining Floxed mouse strains, specific gene knockout or activation is achieved in intestinal epithelial cells (mainly composed of intestinal villi and crypt epithelial cells in the small and large intestines) to study the role of specific genes in intestinal development, barrier function, nutrient absorption, secretion, and homeostasis maintenance. 2. Modeling and Mechanism Exploration of Intestinal Diseases: Construct conditional gene knockout/overexpression models to simulate and study the pathogenesis of intestinal diseases such as inflammatory bowel disease (IBD, such as Crohn's disease, ulcerative colitis), colorectal cancer, and irritable bowel syndrome (IBS). 3. Research on Intestinal Stem Cells and Regeneration: Perform lineage tracing and genetic manipulation in intestinal stem cells and their differentiated descendants to study the self-renewal, differentiation, and regulatory mechanisms of intestinal stem cells in the process of repair after injury. 4. Intestinal Microbiota and Host Interaction: Manipulate related genes in intestinal epithelial cells to study host-microbial interactions, intestinal immunity, and metabolite sensing mechanisms.

1. Research on the gene function of renal distal tubules and collecting duct cells: By combining Floxed mouse strains, time- and cell type-specific gene knockout or activation is achieved in Cdh16 (Cadherin-16, also known as Ksp-cadherin) positive cells (mainly renal distal tubule and collecting duct epithelial cells), for studying the functions of these cells in kidney development, urine concentration, acid-base balance, and maintenance of electrolyte homeostasis. 2. Modeling and mechanism exploration of kidney diseases: Construct conditional gene knockout/overexpression models to simulate and study the pathogenesis of kidney diseases such as polycystic kidney disease, renal tubular acidosis, and nephrogenic diabetes insipidus related to renal distal tubules and collecting ducts. 3. Research on kidney regeneration and repair: By lineage tracing, the proliferation, dedifferentiation, and regeneration repair capacity of Cdh16 positive cells after kidney injury (such as acute kidney injury) are studied.

1. Tracing and functional study of the neural crest cell lineage: Using the Sox10 (SRY-box transcription factor 10) promoter-driven Cre recombinase, specific gene labeling or editing is achieved in neural crest cells and their extensive derivatives (such as Schwann cells, peripheral glial cells, melanocytes, craniofacial mesenchymal cells, adrenal medullary cells, etc.), for the study of neural crest cell migration, differentiation, organogenesis, and related developmental diseases (such as congenital megacolon, Werdnig-Hoffmann syndrome). 2. Development and diseases of the peripheral nervous system: Genetic manipulation is achieved in peripheral glial cells such as Schwann cells and satellite glial cells, to study their roles in peripheral nerve development, myelination, nerve regeneration, and peripheral nerve lesions. 3. Melanocyte biology and melanoma: Gene function studies are conducted in melanocytes and their stem cells, to explore the key mechanisms of their roles in skin pigmentation, melanoma occurrence, development, and metastasis, and to construct hereditary melanoma models.

1. Mesenchymal cell lineage tracing and functional research: Using the Meox2 (Mesenchyme homeobox 2) promoter-driven iCre recombinase, specific gene labeling or editing is achieved in early mesenchymal cells and their derived cells (such as osteoblasts, chondrocytes, cardiomyocytes, skeletal muscle cells, vascular endothelial cells, mesenchymal stem cells, etc.), for studying the role of mesenchymal lineage in embryonic development, tissue and organ formation, and maintenance of homeostasis. 2. Research on heart and vascular development: Genetic manipulation is performed in cardiac progenitor cells, cardiomyocytes, and vascular-related cells to study their differentiation, migration, and function in cardiovascular system development and diseases (such as congenital heart disease, vascular malformations). 3. Research on skeletal and muscle development: Specific knockout or activation of target genes in mesenchymal-derived cells such as osteoblasts, chondrocytes, and skeletal muscle cells is conducted to explore their roles in skeletal development, muscle formation, and related diseases.

1. Research on the function of cell-specific adenosine kinase: By combining tissue-specific Cre-loxP mice, the ADK gene is conditionally knocked out in specific cell types (such as astrocytes, neurons, liver cells, tumor cells) to study the precise regulation of adenosine metabolism reprogramming on intracellular and extracellular adenosine levels, purinergic signaling, and corresponding physiological and pathological processes. 2. Neuroscience and neuroprotection research: Explore how the absence of ADK in astrocytes or neurons can increase extracellular adenosine levels, activate adenosine receptors (such as A1R, A2AR), and thereby affect synaptic transmission, neural excitability, seizure threshold, and neuroprotective mechanisms after ischemic/trumatic brain injury. 3. Tumor metabolism and immunotherapy: Study the impact of ADK functional deficiency in tumor cells or tumor microenvironment on adenosine metabolism, immunosuppressive adenosine accumulation, and antitumor immune responses, and evaluate the potential of targeting the ADK-adenosine pathway in tumor immunotherapy.

1. Fibroblast reticular cell-specific gene function research: By combining Floxed mouse strains, time- and cell type-specific gene knockout or activation is achieved in Ccl19-positive fibroblast reticular cells, for studying the key roles of such stromal cells in the structural formation, maintenance, and immune response regulation of secondary lymphoid organs (such as lymph nodes, spleen, and Peyer's patches). 2. Lymphocyte homing and immune response regulation: Through lineage tracing, the dynamic changes and functions of Ccl19+ stromal cells and their descendants in immune organ development, homeostasis, and inflammatory/tumor states are studied. Explore the functional mechanisms by which Ccl19+ stromal cells regulate the migration, localization, and interactions of immune cells such as T cells and dendritic cells through the secretion of chemokines (such as CCL19, CCL21) and cytokines. 3. Tumor immunology and immunotherapy: The regulatory effects of Ccl19+ stromal cells in lymph tissues such as draining lymph nodes on tumor immune responses are studied, and their potential as new targets for immunotherapy is evaluated.

1. Osteoblast and bone-related cell lineage tracing: Using the Spp1 (osteopontin) promoter-driven Cre recombinase, specific marking or gene editing in osteoblasts and their precursor cells is achieved for studying the cellular mechanisms of bone development, bone homeostasis, bone repair, and bone-related diseases (such as osteoporosis, osteoarthritis). 2. Kidney disease research: Gene manipulation in specific kidney cell types (such as renal tubular epithelial cells, interstitial cells) is achieved for investigating the role of Spp1-expressing cells in acute kidney injury, chronic kidney disease, and renal fibrosis. 3. Immunology and inflammation research: Specific gene manipulation in immune cells such as macrophages and dendritic cells is conducted to study the function of Spp1+ cells in inflammatory responses, tissue repair, and tumor immunomicroenvironment.

1. Research on the Functional Study of Cardiac-Specific Genes: Combined with Floxed mouse strains, conditional gene knockout or activation in cardiomyocytes is achieved to study the role of specific genes in cardiac development, homeostasis maintenance, and disease occurrence (such as myocardial hypertrophy, heart failure, arrhythmias). 2. Cardiomyocyte Lineage Tracing and Fate Tracking: Marking cardiomyocytes and their progeny cells at specific time points (induced by tamoxifen) to study the proliferation, differentiation, and fate of cardiomyocytes during the process of cardiac injury, repair, or regeneration. 3. Cardiac Disease Modeling and Validation of Therapeutic Targets: Constructing mouse models with specific gene modifications in cardiomyocytes to simulate human cardiac diseases and evaluate the efficacy of potential therapeutic strategies (such as gene therapy, drug intervention).

1. Research on the function of cell-specific α-ketoglutarate dehydrogenase (OGDH): Combined with tissue-specific Cre-loxP mice, conditionally knockout the Ogdh gene in specific cell types (such as neurons, liver cells, tumor cells) to study the metabolic and functional consequences of the absence of Odhg, a key node in the tricarboxylic acid cycle (TCA cycle). 2. Exploration of tumor metabolism and therapeutic targets: Investigate the impact of OGDH inactivation in tumor cells on TCA cycle reprogramming, metabolite accumulation (such as α-ketoglutarate), and tumor growth. Assess the potential of targeting the TCA cycle or glutamine metabolism in tumor therapy. 3. Research on the mechanism of neurodegenerative diseases: Study the association between the absence of OGDH function in neurons or glial cells and neuroexcitotoxicity, oxidative stress, and neurodegenerative diseases (such as Alzheimer's disease, Parkinson's disease).

Fibroblast Lineage Tracing and Functional Studies: Achieve specific genetic labeling, knockout, or activation in tissue fibroblasts (particularly cells expressing the type I collagen α2 chain) via tamoxifen induction. Investigate the origin, differentiation, and functional fate of fibroblasts during tissue development, homeostasis maintenance, and injury repair. Tissue Fibrosis Mechanisms and Intervention Research: Study the key role of fibroblasts in the pathogenesis and progression of diseases such as liver fibrosis, pulmonary fibrosis, renal fibrosis, and skin fibrosis. Explore profibrotic signaling pathways and evaluate therapeutic strategies targeting fibroblasts or collagen metabolism. Organ Development and Morphogenesis: Trace the role of fibroblasts in organ formation, structural shaping, and extracellular matrix remodeling. Tumor Microenvironment Research: Investigate the functions of cancer-associated fibroblasts in tumor initiation, progression, metastasis, and therapy resistance.

Cardiac Development Research: Study the fate and function of cardiac progenitor cells and early cardiomyocyte lineages during cardiac morphogenesis, atrioventricular septation, and conduction system formation. Construct heart-specific conditional gene knockout, overexpression, or lineage tracing models to analyze the spatiotemporal-specific functions of particular genes in heart development. Congenital Heart Disease Research: Investigate the molecular mechanisms by which NKX2.5 gene mutations or abnormal downstream target genes lead to congenital heart diseases (e.g., atrial septal defect, tetralogy of Fallot). Cardiomyocyte Regeneration and Repair: Trace the proliferation, regenerative potential of cardiomyocytes in the adult heart, and identify cell sources during injury repair processes. Evaluate the efficacy of therapeutic strategies aimed at promoting myocardial regeneration within specific cell populations. Arrhythmia and Conduction System Disorders: Study the development and function of the cardiac conduction system (e.g., sinoatrial node, atrioventricular node) and explore the cellular and molecular basis of arrhythmias.

Microglia and Central Nervous System Research: Achieve specific gene knockout, knock-in, or reporter gene expression in microglia via tamoxifen induction. Investigate the roles of microglia in neural development, synaptic pruning, neuroinflammation, and neurodegenerative diseases. Track the lineage development, dynamic changes, and functions of microglia in real-time during disease states. Macrophage and Immunology Research: Perform conditional gene editing in macrophages and their precursor cells to study macrophage roles in tissue homeostasis, inflammation, metabolism, and immune regulation. Explore the functions of tumor-associated macrophages in tumor growth, metastasis, and response to immunotherapy. Tissue Repair and Regeneration: Investigate the specific functions of macrophages/microglia in tissue damage repair, regeneration, and fibrosis.

Pancreas Research: Study the molecular mechanisms of pancreatic development, islet cell differentiation, and functional regulation. Establish pancreatic tissue-specific conditional gene knockout or overexpression models. Diabetes Research: Investigate the role of islet β-cell dysfunction and abnormal insulin secretion in the pathogenesis of diabetes. Evaluate the efficacy of strategies aimed at protecting, regenerating, or modulating β-cell function. Pancreatic Cancer Research: Generate genetically engineered mouse models for pancreatic tumors, such as pancreatic ductal adenocarcinoma, to study tumorigenesis and molecular mechanisms.

Neuroscience: Investigate local protein synthesis during synaptic plasticity (e.g., LTP/LTD). Visualize changes in protein synthesis in specific brain regions (e.g., hippocampus, cortex) during learning and memory formation. Explore the mechanisms of dysregulated protein synthesis in neurodegenerative diseases. Cancer Research: Monitor translation activity in cancer cells and stromal cells within the tumor microenvironment in real time. Evaluate the efficacy of anticancer drugs targeting protein synthesis pathways (e.g., eIF4E, mTOR inhibitors).