HKMT Cancer Research Results

HKMT, histone lysine methyltransferase: Click to Expand ⟱
Source:
Type:

HKMT (histone lysine methyltransferase) activity refers to the enzymatic methylation of lysine residues on histone proteins by histone lysine methyltransferases. HKMT enzymes regulate chromatin structure, transcription, cell differentiation, DNA-damage responses and maintenance of cellular identity. Different HKMTs act on distinct histone residues, including H3K4, H3K9, H3K27, H3K36 and H4K20, and can produce either transcriptionally activating or repressive chromatin states depending on the site and degree of methylation. Abnormal HKMT activity is common in cancer and can promote oncogenic transcriptional programs or epigenetic silencing of tumour-suppressive genes. The desired anticancer modulation is therefore enzyme- and context-dependent. HKMT activity is a broad umbrella target of general histone lysine methyltransferase inhibition; specific enzymes such as SUV39H1, EZH2, SETDB1 or G9a/EHMT2.



Scientific Papers found: Click to Expand⟱
7161- CHA,    Chaetocin is a nonspecific inhibitor of histone lysine methyltransferases
- Review, Var, NA
H3K9↓, HKMT↓, SUV39H↓, Dose↝,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

H3K9↓, 1,   HKMT↓, 1,   SUV39H↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  
Total Targets: 4

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: HKMT, histone lysine methyltransferase
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1594  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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