002216 B6.129S7- Rag1 tm1Mom /J Mice homozygous for the Rag1 tm1Mom mutation produce no mature T cells or B cells.

2020年2月10日 · Rag1 knockout (Rag1 KO) mice have been extremely useful to study the role of the immune system in cancer, immunodeficiency disorders, inflammatory conditions, autoimmune diseases, lymphoid tissue pathologies, and graft versus host disease.

034159 C57BL/6J- Rag1 em10Lutzy /J B6J.Rag1 KO is a CRISPR/Cas9 generated knock-out allele of the recombination activating gene 1 locus carrying a 3,527-nt deletion developed at The Jackson Laboratory Rare Disease Translational Center.

2020年2月10日 · A key finding supporting a causal role of the immune system in the pathogenesis of hypertension is the observation that RAG1 knockout mice on a C57Bl/6J background (B6.Rag1 −/ −), which lack functional B and T cells, develop a much milder hypertensive response to Ang II (angiotensin II) than control C57Bl/6J mice.

Rag1 knockout (KO) mice are essential for studying immune system deficiencies, as they lack mature T and B cells. By disrupting V(D)J recombination via the Rag1 gene, these models provide insights into T and B cell development, enabling research …

The Rag1 KO mice (Rag1 knockout) are an immunodeficient stock strain that lack functional B and T lymphocytes. The Rag1 gene (recombination activating gene 1) is crucial for the V(D)J recombination process, which is essential for the development of …

2006年1月1日 · We show here that this approach applied to RAG-1-deficient mice restores normal B- and T-cell function even in the presence of a reduced number of mature B cells. The reconstitution is stable over time, attesting to a selective advantage of transduced progenitors.

003145 C.129S7(B6)- Rag1 tm1Mom /J Mice homozygous for the Rag1 tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" immune deficiency.

1992年3月6日 · RAG-1-deficient mice have small lymphoid organs that do not contain mature B and T lymphocytes. The arrest of B and T cell differentiation occurs at an early stage and correlates with the inability to perform V(D)J recombination.

A key finding supporting a causal role of the immune system in the pathogenesis of hypertension is the observation that RAG1 knockout mice on a C57Bl/6J background (B6.Rag1-/-), which lack functional B and T cells, develop a much milder hypertensive response to Ang II (angiotensin II) than control C57Bl/6J mice.