Dette kan du ikkje gå glipp av! Sjekk berre desse abstracta:
det populærvitskaplige
Identifisering av nye proteinfaktorar som er viktige for celledød og cellevekst.
Kristian K. Starheim, PhD-student, Institutt for kirurgiske fag, Universitetet i Bergen. kristian.starheim@mbi.uib.no
Kreftceller er celler som veks ukontrollert. Sjølv om vi no veit mykje om cellene i kroppen, er det svært mykje vi ikkje enda veit.
Det er viktig å forstå cellevekst for å forstå kreft. Denne kunnskapen kan vi bruke til å utvikle betre kreftmedisinar med færre biverknader.
Vi har funne to kompleks i menneskeceller, som begge er nødvendige for at eller skal vekse normalt. Vi håpar vidare å utvikle medisinar som kan påverke desse kompleksa.
Objective:
To identify the novel co-translational human N-a-acetyltransferase complexes hNatB
and hNatC.
Conclusions:
We here present the novel human NatB and NatC complexes (hNatB and hNatC).
hNatB consists of the predicted N-acetyltransferase hNat3, and the auxiliary subunit
hMdm20, while hNatC consists of the N-acetyltransferase hMak3, and the auxiliary
subunits hMak10 and hMak31. Both complexes are conserved from yeast with respect
to subunit composition, substrate specificity and ribosome binding. hNatB was found
to acetylate peptides with N-termini Met-Asp-, while hNatC acetylates peptides with
N-termini Met-Leu-.
Knockdown of hNatB subunits disrupts normal cell cycle progression, and induces
growth inhibition in HeLa cells and the thyroid cancer cell line CAL-62.
Knockdown of hNatC subunits results in reduced growth and disturbed cell cycle
progression in HeLa cells. Knockdown of hMak3 leads to p53-dependent cell death,
and aberrant localization of the Arf-like GTPase hArl8b.
Taken together, these studies emphasize the importance of N-a-terminal acetylation for
normal cell function in eukaryotic cells.
This work was supported by The Norwegian Cancer Society, The L. Meltzer
Foundation, Norwegian Health Region West, and the Norwegian Research Counsil.
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