Although excessive fibroblast proliferation and inflammation occur when abnormal remodeling occurs, genes that regulate repair remain unknown.
The roles of MMP7 in regulating repair and inflammation are particularly prominent in the lungs.
At the transcriptional level, the E2F transcription factors have been known to play a role in regulating repair proteins.
In other organisms this represents a typically small group of essential kinases that regulate repair, morphogenesis, and differentiation and are named after their ability to phosphorylate casein.
Bone morphogenetic proteins are important for regeneration/repair of the dentin-pulp complex after cariogenic injury [ 33], and BMP4, in particular, has been shown to initiate and regulate repair of carious tissue [ 34, 35].
The observation that over-expression of ectopic 14-3-3σ 14-3-3σ 14-3-3σ knockincreasesits expression reduces resistance to gemcitabine, suggests that 14-3-3σ may also play a role in regulating repair of premature terminations.
Hepatocyte growth factor (HGF /c-Met and transforming growtHGF /c-Met (TGF-α)/epidermandgrowtransformingceptor (Egrowthre well known to regulate repair of damaged alveolar epithelium by stimulating cell migration and proliferation.
Another RTK, c-Met, and its ligand hepatocyte growth factor (HGF) are also well known to regulate repair of damaged epithelium by stimulating cell migration, proliferation, and survival (14, 17, 25, 27, 34).
Consistent with these observations, a recent study showed that a class III HDAC (SIRT6) positively regulated the repair of double-strand breaks (DSBs) through deacetylation of CtIP [ 21].
Recent studies show that survivin interacts with components of DNA double-strand break repair and might regulate DNA repair [ 44].
