B6-huKIT Mouse
Product Name
B6-huKIT Mouse
Product ID
C001899
Strain Name
C57BL/6NCya-Kittm3(hKIT)/Cya
Backgroud
C57BL/6NCya
Status
When using this mouse strain in a publication, please cite “B6-huKIT Mouse (Catalog C001899) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Name
KIT
Gene Alias
PBT, SCFR, C-Kit, CD117, MASTC
NCBI ID
Chromosome
Chr 4 (Human)
MGI ID
Datasheet
Strain Description
KIT (also known as c-Kit or CD117) is a type III receptor tyrosine kinase proto-oncogene located on chromosome 4q12, originally identified as the cellular homolog of the feline sarcoma virus v-kit. Upon binding to its ligand stem cell factor (SCF), KIT activates downstream signaling cascades that regulate cellular proliferation, differentiation, migration, and apoptosis [1]. KIT plays essential roles in hematopoiesis, stem cell maintenance, gametogenesis, melanogenesis, and mast cell development and function. KIT is prominently expressed in hematopoietic stem cells, mast cells, melanocytes, germ cells (up to the pachytene stage), and interstitial cells of Cajal in the gastrointestinal tract. Its protein product is readily detectable via immunohistochemistry. CD117 is widely used in diagnostic pathology to label tissues such as bone marrow (hematopoietic progenitors), skin (mast cells and melanocytes), gastrointestinal stroma (Cajal cells), and testis (germ cells). Mutations in KIT are implicated in a spectrum of diseases, including gastrointestinal stromal tumors (GIST), systemic mastocytosis, acute myeloid leukemia, seminoma, and vitiligo. These mutations often contribute to the persistence of cancer stem cells and therapeutic resistance [1-2]. Clinically approved tyrosine kinase inhibitors (TKIs) such as imatinib, sunitinib, regorafenib, ripretinib, and avapritinib selectively target KIT mutations and are used in the treatment of GIST and mast cell disorders. Ongoing research is advancing next-generation inhibitors, combination therapies, antibody-drug conjugates, and ligand-directed delivery strategies to expand the therapeutic scope of KIT-targeted interventions and support precision medicine approaches [3-4].
The B6-huKIT mouse is a humanized model generated by replacing the endogenous murine Kit gene with the human KIT coding sequence via gene editing. This model enables investigation of the molecular pathogenesis of human KIT mutations in relevant disease contexts, preclinical evaluation of TKIs and emerging therapies, and functional studies of KIT in hematopoietic stem cells, melanocytes, and mast cells.
Reference
Miettinen M, Lasota J. KIT (CD117): a review on expression in normal and neoplastic tissues, and mutations and their clinicopathologic correlation. Appl Immunohistochem Mol Morphol. 2005 Sep;13(3):205-20.
Sheikh E, Tran T, Vranic S, Levy A, Bonfil RD. Role and significance of c-KIT receptor tyrosine kinase in cancer: A review. Bosn J Basic Med Sci. 2022 Sep 16;22(5):683-698.
Rivonker SC, Nada H, Jaemin C, Kwon YJ, Lee K. c-KIT Small Molecule Inhibitors as a Therapeutic Strategy for Melanoma: Clinical Insights, SAR, and Future Directions. Arch Pharm (Weinheim). 2025 Oct;358(10):e70113.
Tomuleasa C, Tigu AB, Munteanu R, Moldovan CS, Kegyes D, Onaciu A, Gulei D, Ghiaur G, Einsele H, Croce CM. Therapeutic advances of targeting receptor tyrosine kinases in cancer. Signal Transduct Target Ther. 2024 Aug 14;9(1):201.
Strain Strategy
Figure 1. Gene editing strategy of B6-huKIT mice. The mouse Kit DNA was replaced with the human KIT DNA. The murine signal peptide was preserved.
Application Area
Mechanistic studies of KIT mutation–driven mast cell hyperplasia and systemic mastocytosis;
Functional analysis of KIT mutations in GIST initiation, invasion, and metastasis;
Investigation of hematopoietic stem cell self-renewal and differentiation, melanocyte biology, and melanoma pathogenesis;
Preclinical evaluation of KIT-targeted TKIs and novel therapeutic strategies, including resistance mechanisms.
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