Tuesday, May 24, 2016

My earlier notes

  1. Histone methylation vs DNA methylation
DNMT3a3b vs PRC1/2.
DNA methylation degrades bivalent chromatin
Epigenetic drift

2. DNA methylation better predictor of chronological age than telomerase

3. DNMT3a

4. Bivalent chromatin
Bivalent promoters control hundreds or thousand genes, differentiation and tissue specific

5. Cancer DNA methylome

PCR2 during embryonal stem cell differentiation

DNA methylation and histone meth in aging mouse HSCs, very thorough
p16INK4a not upregulated in old stem cell

HSC renewal caused by DNMt3a mutation (effectively knock down)  induces leukemia

9. melatonin and aging

10. Tissue maintenance

11. Epigenetic dysregulation, stem cells

12. Aging and epigenetic drift
13.  review on dna methylation

14. review on histone methylation

Age-Associated Hyper-Methylated Regions in the Human Brain Overlap with Bivalent Chromatin Domains
16. hsc exhaustion by methylation of prc2 targets

17. Tumor microenvironment immune suppression is PTEN dependent

18. epigenetic deregulation is a common feature of aging in mammals

19. DNMT1 decreases with aging, citations

20. Aging and DNA methylation. Very good

21. chromatin in aging and cancer (methylation, histones, ncRNA)

Transcriptome landscape in human genome

23. Partial hepatectomy, lncRNA regulates regeneration

24. Long non coding RNA really like to guide PRC2

25. surprise, aging can impair regeneration of liver

Epigenetic regulation of ageing: linking environmental inputs to genomic stabilit

Very good
free on researchgate
it’s the chromatin, stupid!

26. Mouse strains survival curves

27. Naked mole rate sequencing

Cellular senescence and the senescent
secretory phenotype: therapeutic opportunities

Adult ‐ onset, short ‐ term dietary restriction reduces cell senescence in mice

Insulin-like growth factor-1 regulates the SIRT1-p53 pathway in
cellular senescence

Regulation of p16/INK4 (PRC2 and histone modification involved)

PRC2 meets senescence

33. p16 hypermethylation increases age related cancer incidence in mice
seems like the epigenetic dysregulation of the genome, which upregulates many sequences, also upregulatesp16 thus inherently protecting against cancer -> lowering the threshold toward degenerating into senescencent phenotype

is there anything that drives epigenetic dysregulation or is it just enthropy?

34. or histone deacethylase??

35. Good thorough paper on time restricted feeding in mice. Unfortunately no lifespan or health span investigation, only biomarkers. Very good effects on serum insulin and cholersterol.

36. mTOR regulates circadian rythm?

37. Transposable elements drive ageing

38. mtDNA mutations in oocytes are much less frequent than in somatic cells

While somatic cells depend mostly on mitochondrial oxidative phosphorylation (OxPhos), pluripotent stem cells possess immature mitochondria and preferentially use glycolysis as their major source of energy

DNA demethylation

41. Overexpression DNMR3b1 but not DNMT3a1 of cancer prone trangenic mice increases tumor incidence. Same pathway (igf2 overexpression by suppressing H19) as in DNMT1 overexpression study,
Maybe DNMT3a can be overexpressed without adverse effects?
The article has a nice inrroduction where they state the cancer cells are generally hypomethylated byt hypermethylated at PRC2 binding sites. This is exactly the same as the findings about aging stem cell.

42. Adult stem cell epigenetics, very good

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