Glucagon receptor knockout mice were previously generated by homologous recombination in embryonic stem cells on a DBA/1LacJ background [ 2].
Sgca null, Nfix null, mdx, and Tg Mlc1f-Nfix2 mice were previously described17, 26, 35, 42.
Gal3−/− mice were previously generated as described and bred on the C57BL/6 mouse background for nine generations48.
(B-D) C57BL/6 mice were previously treated with CD39 (ARL67156, 2 mg.kg−1, CD39i) or CD73 [adenosine 5′- α,β-methylene) diphosphate, 4 mg.kg−1, CD73i] inhibitors 1 h before administration of FBP (100 mg.kg−1).
P2×7-deficient mice were previously shown to exhibit an osteopenic phenotype and abnormal fat distribution, leading us to hypothesize that P2×7R activation was involved in the differentiation of BMSCs.
CCSP-rtTA mice were previously described [23].
Cln3Δex7/8 mutant mice were previously described [32].
K14-TSLP transgenic, IL-7Rα−/− [70] and Msx2Cre mice were previously described [7], [71].
Transgenic Lck-Bax mice were previously described and genotyped by PCR method [8].
Heparanase overexpressing C57BL/6 transgenic (hpa-tg) mice were previously described in detail [40].
MCP-1 mice were previously described [33], which were purchased from the Jackson Laboratory.
