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Table 1 Major splicing regulators involved in adipogenesis processes of white, brown, and beige adipose tissues

From: Regulatory roles and mechanisms of alternative RNA splicing in adipogenesis and human metabolic health

Splicing regulators Phenotypes in transgenic animals Splicing targets Splicing effects References
Sam68 The Sam68-KO(knockout) mice: a lean phenotype with reduced body weight and adiposity; WAT browner; increased thermogenesis; reduced lipid stores in BAT; improved insulin sensitivity; abnormal neuronal processes; defective spermatogenesis and osteogenesis mTOR;
Enhance WAT adipogenesis;
impair browning trans-differentiation
FTO 1. The FTO-KO mice: increased postnatal lethality; a lean phenotype; postnatal growth retardation; decreased adiposity; increased energy expenditure
2. The FTO-overexpression mice: obesity with an increase in fat mass; hyperphagia; marked glucose intolerance
RUNX1T1 Enhance WAT adipogenesis [75,76,77,78,79]
SRSF10 The SRSF10-KO mice: multiple cardiac defects; severely impaired WAT development in embryos LPIN1;
Enhance WAT adipogenesis [80,81,82]
RBM4 The RBM4a-KO mice: impaired development of BAT, muscles, and pancreatic β-islets; hyperlipidemia PRDM16; MBNL1
BAT splicing cascades: RBM4a-SRSF3-MAP4K4; RBM4-MEF2C; RBM4-Nova1-SR-SF6; RBM4-SRPK1; RBM4-Acin1-SRSF3
Enhance BAT adipogenesis [62, 63, 83,84,85,86,87,88]