In mammals, mitochondria act as the central checkpoints for many forms of apoptosis.
Thus, LasR represents a central checkpoint with the highest degree of interconnection in the network [ 10, 11].
The mammalian target of rapamycin (mTOR) constitutes a central checkpoint that suppresses autophagy via restraining the kinase activity of UNC-51-like kinase (ULK1) [ 102, 103].
As described above, despite the extensive negative selection of B cells both in the BM at a central checkpoint and at a peripheral checkpoint, a substantial portion of autoreactive specificities remain present in the peripheral B-cell pool.
They both rely on the central checkpoint kinase Rad3, the fission yeast homolog of human ATR and budding yeast Mec1, and the downstream checkpoint effector kinase Cds1, homolog of Chk2 and Rad53.
For a strain that lacks all three functions of the checkpoints, we used rad3Δ, which lacks the central checkpoint kinase.
The regulation of the mitochondria intrinsic pathway is performed by a complex protein network in which the B-cell lymphoma protein-2 (Bcl-2) family members form a central checkpoint that determines whether a cell lives or dies [20].
A number of genes influence the level of these autoreactive B cells and whether they are eliminated or not during development at a central checkpoint in the bone marrow (BM) or at a later checkpoint in peripheral lymphoid tissues.
Just how AID functions to regulate the central checkpoint in the BM is unclear.
Because of the role of AMPK as a central energy checkpoint in the cell, these findings link LKB1 signaling to energy metabolism control, positioning LKB1 as a critical mediator of the effects of low energy on cell viability11, 13.
