Overview of knockout or knock-in mouse models of TGF-β-associated protein

Knockout mouse modelPhenotypeReference
Smad5Embryonic fatal; faulty vascular development, ventral closure, cardiac development, and craniofacial development; aberrant heart looping and embryonic turning[111, 112]
Smad3A reduced size compared to littermate controls[15, 113]
Smad7Body sizes were smaller than wild-type mice[114]
Activin βANewborn fatality; cranial defects (cleft palate and loss of whiskers, upper incisors, lower incisors, and lower molars)[115, 116]
Activin βBLarge litters but delayed parturition; breastfeeding issues; birth abnormalities in eyelid closure[117]
Activin βCNo noticeable abnormalities; viable[118]
Activin βENo noticeable abnormalities; viable[118]
Activin βB knockin to the activin βA locusReversal of activin A-deficient neonatal mortality. Defects in the development of the hair, gonads, external genitalia, and somatic growth[119]
Growth differentiation factor 9 (GDF-9)Viable; female infertility; one-layer primary follicle stage halt of folliculogenesis[120, 121]
Inhibin αFemale infertility; secondary male infertility; granulosa/Sertoli cell and adrenal tumors; cachexia-like condition[122]
Activin receptor type IIInfertility in females is caused by a folliculogenesis abnormality; delayed fertility in males; undersized gonads; 25% of mice die at birth owing to mandible deformities[116]
FKBP12Due to cardiomyopathy and neural tube abnormalities, the majority of mice perish between embryonic day 14.5 (E14.5) and delivery[123]
FollistatinNeonatal fatality; craniofacial abnormalities, development retardation, and skin abnormalities[111]