huKIT Mouse
製品名
huKIT Mouse
製品ID
C001899
系統名
C57BL/6NCya-Kittm3(hKIT)/Cya
背景情報
C57BL/6NCya
状況
このマウス系統を論文で使用する場合は、「huKIT Mouse（カタログ番号C001899）はサイアジェンから購入しました。」と引用してください。
製品タイプ
年齢
遺伝子型
性別
数量
遺伝子名
遺伝子別名
PBT, SCFR, C-Kit, CD117, MASTC
NCBI ID
染色体
Chr 4
MGI ID
さらに
系統詳細
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 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.
参考文献
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.
系統作製戦略
The mouse Kit DNA was replaced with the human KIT DNA. The murine signal peptide was preserved.
Figure 1. Gene editing strategy of huKIT mice.
適用分野
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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