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SUMMARY:You get a methylation\, and you get a methylation\, everybody gets
  a methylation - Dr Pedro J Batista\, NIH\, Center for Cancer Research\, B
 ethesda\, MC\, USA
DTSTART:20221122T140000Z
DTEND:20221122T150000Z
UID:TALK177566@talks.cam.ac.uk
CONTACT:Lynn Froggett
DESCRIPTION:The tricarboxylic acid cycle is a central metabolic pathway us
 ed by organisms to generate energy\, as well as providing biomolecular bui
 lding blocks. Mutations in TCA cycle enzymes are a known driver of specifi
 c cancer types. One example is loss of function of the fumarate hydratase 
 enzyme in hereditary leiomyomatosis and renal cell cancer. Accumulation of
  fumarate has previously been shown to inhibit α-ketoglutarate (aKG)-depe
 ndent dioxygenases involved in DNA and histone demethylation\, however\, t
 he link between fumarate accumulation and the epitranscriptome is unclear.
  We evaluated the effects of fumarate accumulation on different members of
  the (aKG)-dependent dioxygenases which act upon RNA modifications. We fin
 d that fumarate accumulation has a greater effect on the demethylases that
  act upon N6-methyladenosine (m6A)\, and that other RNA demethylases are u
 naffected. Our results suggest that metabolic rewiring in HLRCC impacts di
 fferent RNA modifications to different extent\, leading to changes in gene
  expression that might support disease progression.
LOCATION:Virtual
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