I began convinced that if I dug deeply enough into their character, I would understand why Columbine happened — that I would recognize damage in their household that spilled over into catastrophe.
Upon DNA damage, XPC and HR23B recognize damage site, XPA verifies, XPB and XPD unwind DNA double strands, finally XPF and XPG excise the damaged strand.
TLRs act as sentinels not only for PAMPs, but also recognize damage-associated molecular patterns (DAMPs) from dead and damaged cells and tissues, resulting in inflammation (Sangiuliano et al., 2014).
Among the different PRRs, Toll-Like Receptors (TLRs) are able to recognize Damage-Associated Molecular Patterns (DAMPs) produced by injured tissues and damaged and activated cells, thus playing a putative role in tissue homeostasis and repair such as postradiation exposure [ 50].
DNA glycosylases can recognize damaged bases and remove them via cleavage of the N-glycosidic bond to initiate BER.
Many recent studies also indicate that natural IgM can recognize damaged-self such as late apoptotic or necrotic cells in various tissues [14], [18], [19], [20], [21].
In S. cerevisiae there are at least five distinct DNA glycosylases, namely Ung, Nth1, Nth2, Ogg1, and Mag, that collectively recognize damaged bases and process them to generate abasic sites.
These receptors recognize damage-associated molecular patterns (DAMPs), which are either derived from pathogens (pathogen-associated molecular patterns, or PAMPs) or are self-proteins (stress or danger-associated molecular patterns, or SAMPs) [ 14, 15].
TLRs recognize damage-associated molecular patterns and activate nuclear factor kappa light-chain-enhancer of activated B cells (NF-κB), which initiate the production of numerous cytokappa light-chain-enhancerecules.
The contact factors of the intrinsic clotting system recognize damaged host cell membranes, foreign substances, (particularly negatively charged molecules, including lipids such as bacterial LPS), and abnormalities along endothelial surfaces [ 1, 2, 26].
Such systems generally (i) have the ability to selectively recognize damaged or misfolded proteins, (ii) target a broad array of misfolded substrates for refolding or degradation, (iii) undergo induction or activation in response to proteotoxic stress, and (iv) protect cells from possible cell death in the presence of proteotoxic stresses.
