HIGHLIGHTS
SUMMARY
Differentiation and senescence, through permanent removal of post-translational modifications from histone proteins (Duarte et_al, 2014; Azad et_al, 2018; Cheung et_al, 2021; Ferrari et_al, 2021). The cystatin B (CSTB) protein has been characterized in detail as an endogenous inhibitor of lysosomal cysteine cathepsins (Stubbs et_al, 1990; Turk and Bode, 1991). In contrast, biallelic total loss-of-function CSTB mutations cause a neonatal-onset developmental encephalopathy with progressive microcephaly (Mancini et_al, 2016; O`Brien et_al, 2017). Previous studies have shown that the presymptomatic phase in Cstb-/- mice is characterized by microglial activation and dysfunction, reduced . . .
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