MRL/MpJ-Fas-KO Mouse
製品名
MRL/MpJ-Fas-KO Mouse
製品ID
C001602
系統名
MRL/MpJ-Fasem1/Cya
背景情報
MRL/MpJ
状況
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製品タイプ
年齢
遺伝子型
性別
数量
遺伝子名
遺伝子別名
lpr, APO1, APT1, CD95, TNFR6, Tnfrsf6
NCBI ID
染色体
Chr 19
MGI ID
--
さらに
系統詳細
The Fas cell surface death receptor (FAS), also known as CD95 or TNFRSF6, is a type I transmembrane protein in the tumor necrosis factor receptor superfamily [1]. It plays a key role in apoptosis by transmitting signals that initiate programmed cell death. Expressed across various tissues such as immune cells, liver, heart, and skin, FAS regulates cellular homeostasis. Upon binding with its ligand (FASL), FAS oligomerizes to form the death-inducing signaling complex (DISC), activating caspases that execute apoptosis. This is crucial for immune homeostasis, tissue maintenance, and removing damaged or infected cells. Dysregulated FAS-mediated apoptosis can lead to autoimmune disorders (e.g., autoimmune lymphoproliferative syndrome) or contribute to cancer development by enabling uncontrolled cell proliferation [1-3].
The MRL/MpJ Strain (Murphy Roths Large), derived from a complex cross between several strains (LG/J, AKR/J, C3H/Di, C57BL/6), was established for autoimmune disease research. They serve as controls in studies of the MRL/MpJ-Faslpr strain, a mouse model with premature termination of gene transcription and abnormal mRNA splicing due to lymphoproliferation (lpr) spontaneous mutation of the Fas gene, which develops lupus-like autoimmune disease [4]. MRL/MpJ mice are vital in studying autoimmune conditions (e.g., Sjögren syndrome, autoimmune arthritis, lupus erythematosus, hearing defects) and are notable for their scarless tissue regeneration capabilities. This makes them valuable models for research in tissue regeneration, wound healing, autoimmune diseases, muscle dystrophy, and hearing loss [4-6].
The MRL/MpJ-Fas knockout (KO) mouse model, generated via targeted deletion of the Fas gene in MRL/MpJ mice, provides a critical tool for investigating the role of FAS in autoimmune pathologies. This model furnishes a critical system for elucidating the etiology of systemic lupus erythematosus (SLE) and identifying potential therapeutic targets within the FAS signaling cascade for the treatment of autoimmune disorders.
参考文献
Volpe E, Sambucci M, Battistini L, Borsellino G. Fas-Fas Ligand: Checkpoint of T Cell Functions in Multiple Sclerosis. Front Immunol. 2016 Sep 27;7:382.
Opferman JT. Apoptosis in the development of the immune system. Cell Death Differ. 2008 Feb;15(2):234-42.
de Oliveira GL, Malmegrim KC, Ferreira AF, Tognon R, Kashima S, Couri CE, Covas DT, Voltarelli JC, de Castro FA. Up-regulation of fas and fasL pro-apoptotic genes expression in type 1 diabetes patients after autologous haematopoietic stem cell transplantation. Clin Exp Immunol. 2012 Jun;168(3):291-302.
Adachi M, Watanabe-Fukunaga R, Nagata S. Aberrant transcription caused by the insertion of an early transposable element in an intron of the Fas antigen gene of lpr mice. Proc Natl Acad Sci U S A. 1993 Mar 1;90(5):1756-60.
Heydemann A. The super super-healing MRL mouse strain. Front Biol (Beijing). 2012 Dec 1;7(6):522-538.
Velasco C, Dunn C, Sturdy C, Izda V, Martin J, Rivas A, McNaughton J, Jeffries MA. Ear wound healing in MRL/MpJ mice is associated with gut microbiome composition and is transferable to non-healer mice via microbiome transplantation. PLoS One.
系統作製戦略
The sequence of exons 2-4 of the Fas gene was knocked out in MRL/MpJ mice by gene editing technology.
Figure 1. Gene editing strategy for MRL/MpJ-Fas-KO mice.
適用分野
Systemic Lupus Erythematosus (SLE) research;
Immunology and inflammation-related research;
Other autoimmune research (Sjögren’s syndrome, Rheumatoid Arthritis, etc.).
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