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In view of this body of evidence, it is plausible that the ECM is responsible for maintaining tissue regulation under normal conditions.
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This is clearly exemplified by the fact that clusters of silent genes are mainly stable during differentiation and contain genes involved in development or function of non-hematopoietic organs, thus indicating the involvement of positional gene expression regulation in maintaining tissue specific patterns of expression.
The regulation of gene expression is important in maintaining tissue homeostasis, preventing inflammatory processes and cancer.
In conclusion, we hypothesize that TPPP1 is an important enforcer of the cell cycle checkpoints and that correct regulation of its activity may be important for maintaining tissue homeostasis.
One suite of the molecular mechanisms that results in the removal of highly compromised symbionts from stressed host tissues involves regulation of cell death pathways which play active roles in maintaining tissue homeostasis and immune responses [2], [6], [10], [11].
This tight regulation is essential for proper morphogenesis during embryo development and for maintaining tissue and organ structure homeostasis in the adult [ 5, 6].
Androgens, apart from maintaining tissue homeostasis and controlling secretory function of prostatic epithelium, play a major role in the regulation of prostate development and differentiation before birth and during puberty.
The innate immune system plays an important role in tissue repair and in maintaining tissue homeostasis.
The endothelial-blood/tissue barrier is critical for maintaining tissue homeostasis.
In physiological conditions, PTEN maintains tissue homeostasis by coordinated regulation of polarised cell growth (Kolsch et al, 2008) and morphogenesis (Martin-Belmonte et al, 2007), as well as cell death (Weng et al, 2001).
Collagen plays a major part in organizing and maintaining tissues.
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