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Noncoding RNA Activated by DNA Damage (NORAD) is a long non-coding RNA that responds to DNA damage and plays a significant role in preserving stability (keeping it accurate and unchanged) of genetic information within cells. [2] Upon DNA damage, the amount of NORAD increases within cells and work to prevent proteins responsible for stabilizing ...
Cells with a defective G 2-M checkpoint will undergo apoptosis or death after cell division if they enter the M phase before repairing their DNA. [1] The defining biochemical feature of this checkpoint is the activation of M-phase cyclin-CDK complexes, which phosphorylate proteins that promote spindle assembly and bring the cell to metaphase. [2]
After DNA damage, cell cycle checkpoints are activated. Checkpoint activation pauses the cell cycle and gives the cell time to repair the damage before continuing to divide. DNA damage checkpoints occur at the G1/S and G2/M boundaries. An intra-S checkpoint also exists. Checkpoint activation is controlled by two master kinases, ATM and ATR.
For example, TLR2-agonistic DAMPs activate renal progenitor cells to regenerate epithelial defects in injured tubules. TLR4-agonistic DAMPs also induce renal dendritic cells to release IL-22, which also accelerates tubule re-epithelialization in acute kidney injury. Finally, DAMPs also promote renal fibrosis by inducing NLRP3, which also ...
The negative feedback loop used to successfully inhibit the inhibitor, p27, is another essential process used by cells to ensure mono-directional movement and no backtrack through the cell cycle. When DNA damage occurs, or when the cell detects any defects which necessitate it to delay or halt the cell cycle in G1, arrest occurs through several ...
When DNA is damaged such as due to a lesion, a complex signal transduction pathway is activated which is responsible for recognizing the damage and instigating the cell's response for repair. Compared to the other lesion repair mechanisms, DDR is the highest level of repair and is employed for the most complex lesions.
The inflammasome was discovered by the team of Jürg Tschopp, at the University of Lausanne, in 2002. [17] [18] In 2002, it was first reported by Martinon et al. [17] that NLRP1 (NLR family PYD-containing 1) could assemble and oligomerize into a structure in vitro, which activated the caspase-1 cascade, thereby leading to the production of pro-inflammatory cytokines, including IL-1β and IL-18.
When there is too much damage, apoptosis is triggered in order to protect the organism from potentially harmful cells.7 p53, also known as a tumor suppressor gene, is a major regulatory protein in the DNA damage response system which binds directly to the promoters of its target genes. p53 acts primarily at the G1 checkpoint (controlling the G1 ...