Disease relevance of Capn5

• There was no evidence for the development of autoimmune disease in Capn5-null animals [1].
• On the other hand, the specific downregulation of heart development-related genes (e.g., notch gene homolog-1, MAD homolog-4) and the upregulation of proteolysis genes (e.g., calpain-5) in the CIH heart can explain the lack of hypertrophy in CIH [2].

High impact information on Capn5

• In the thymus, Capn5 was expressed mainly in relatively immature CD25(+) embryonic thymocytes [1].
• Capn5 is expressed in a subset of T cells and is dispensable for development [1].
• There were no defects in the major T- or B-cell populations in the thymus, spleen, bone marrow, or peritoneum, nor did apoptosis appear abnormal in Capn5-null T cells [1].
• The Capn5 gene was inactivated by homologous recombination in ES cells that subsequently colonized the germ line of mice [1].
• Refined mapping of Capn5, also previously localized to chromosome 7, indicated that it was not closely linked to Capn12, mapping tightly linked to a marker positioned at 48.5 cM [3].

Biological context of Capn5

• The major expression sites of Capn5 during embryogenesis are the developing thymus, sympathetic and dorsal root ganglia [4].

Anatomical context of Capn5

• Both genes are differentially expressed in human tissues with highest RNA levels for Capn5 occurring in the testis, liver, trachea, colon, and kidney, while Capn6 is highly expressed only in the placenta sample of the 50 tissues examined [5].

Other interactions of Capn5

• Here we report the mRNA expression patterns during mouse development of the recently identified Capn5, Capn6 and Capn11 genes [4].

References