BioAcyl Corp
BioAcyl Corp |
|
 |
 |
 |
|
Meng, S., Chanda, P., & Thandavarayan, R. A. (2018). Transflammation: How Innate Immune Activation and Free Radicals Drive Nuclear Reprogramming. Antioxidants & Redox Signaling, 29(2), 205–218. Added by: Dr. Enrique Feoli (21/05/2023, 18:57) Last edited by: Dr. Enrique Feoli (13/10/2023, 15:58) |
 |
| Resource type: Journal Article DOI: 10.1089/ars.2017.7364 ID no. (ISBN etc.): 1523-0864 BibTeX citation key: Meng2018 View all bibliographic details  |
Categories: BioAcyl Corp, BioAcyl Corp Subcategories: Stemness, Transflammation Creators: Chanda, Meng, Thandavarayan Collection: Antioxidants & Redox Signaling |
Views: 6/112
|
| Abstract |
|
Significance: Yamanaka and colleagues galvanized the field of stem cell biology and regenerative medicine by their generation of induced pluripotent stem cells. Evidence is emerging that activation of innate immune signaling is critical for efficient reprogramming to pluripotency and for the nuclear reprogramming occurring in transdifferentiation., Recent Advances: We have shown that innate immune signaling triggers a global change in the expression of epigenetic modifiers to enhance DNA accessibility. In this state of epigenetic plasticity, overexpression of lineage determination factors, and/or environmental cues and paracrine factors, can induce pluripotency, or can direct transdifferentiation to another somatic cell lineage. Accumulating evidence reveals that innate immune activation triggers the generation of reactive oxygen species and reactive nitrogen species, and that these free radicals are required for nuclear reprogramming to pluripotency or for transdifferentiation., Critical Issues: We have discovered a limb of innate immune signaling that regulates DNA accessibility, in part, by the action of free radicals to induce post-translational modification of epigenetic modifiers., Future Directions: It is of scientific interest and clinical relevance to understand the mechanisms by which free radicals influence epigenetic plasticity, and how these mechanisms may be therapeutically modulated. Antioxid. Redox Signal. 29, 205–218.
|