CURRICULUM VITAE SFEIR

The latter refers to the propensity of linear chromosome ends to be recognized as DNA double stranded breaks. Non-telomeric role for Rap1 in regulating metabolism and protecting against obesity. Journal of Cell Science. The former stems from the inherent inability of the replication machinery to fully duplicate linear templates. Our lab is mainly interested in understanding the basic mechanism that leads to telomere length resetting. To surmount both problems, cells use telomeres, the specific nucleoprotein complexes that are essential to ensure genomic stability and promote cellular survival.

Telomeres at a glance. PhD from Southwestern University. Opens in a new tab. Normal human somatic cells lack the activity of telomerase and gradually loose telomeric repeats during progressive division cycles until they ultimately undergo cellular senescence. Mammalian polymerase theta promotes alternative-NHEJ and suppresses recombination. The latter refers to the propensity of linear chromosome ends to be recognized as DNA double stranded breaks. Associate Professor, Department of Cell Biology.

Associate Professor, Department of Cell Biology.

Our lab is mainly interested in understanding the basic mechanism that leads to telomere length resetting. Non-telomeric role for Rap1 in regulating metabolism and protecting against obesity. A second area of their interest is to understand how telomere dynamics impact stem cell function and leads to tumorigenesis, using the mouse as a model organism.

  BARBIE DOLL MARGE PIERCY THESIS STATEMENT

Agnel Sfeir | Blavatnik Awards for Young Scientists

Journal of Cell Science. See All Publications Mammalian polymerase theta promotes alternative-NHEJ and suppresses recombination. The linearity of chromosomes creates two major problems for eukaryotic cells: Normal human somatic cells lack the activity steir telomerase and gradually loose telomeric repeats during progressive division cycles until they ultimately undergo cellular senescence.

Normal human somatic cells lack the activity of telomerase and gradually loose telomeric repeats during progressive division cycles until curricilum ultimately undergo cellular senescence.

curriculum vitae sfeir

PhD from Southwestern University. The linearity of chromosomes creates two major problems for eukaryotic cells: A second area of interest to us is to understand how telomere dynamics impact stem cell function and leads to tumorigenesis, using the mouse as a model organism.

Victor Petrus Sfeir

Stop pulling my strings – what telomeres taught us about the DNA damage response. To vitze both problems, cells use telomeres, the specific nucleoprotein complexes that are essential to ensure genomic stability and promote cellular survival. Agnel Sfeir is mainly interested in understanding the basic mechanism that leads to telomere length resetting. Telomeres are replenished by telomerase, a reverse transcriptase that is active in the germ line and during early embryonic currixulum.

Areas of Research Interest and Expertise: To surmount both problems, cells use telomeres, the specific nucleoprotein complexes that are essential to ensure genomic stability and promote cellular survival. Telomeres at a glance.

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curriculum vitae sfeir

Opens in a new tab. In particular, we rely on nuclear reprograming as a platform to identify factors that regulate telomere length. Telomeres are replenished by telomerase, a reverse transcriptase that is active in the germ line and during early embryonic development.

The former stems from the inherent inability of the replication machinery to fully duplicate linear templates. The latter refers to the propensity of linear chromosome ends to be recognized as DNA double stranded breaks.

Laura Metzler | American University of Beirut –

The latter refers to the propensity of linear chromosome ends to be recognized as DNA double stranded breaks. Is this your profile?

curriculum vitae sfeir

Stressed telomeres without POT1 enhance tumorigenesis [Editorial]. Polymerase theta is a robust terminal transferase that oscillates between three different mechanisms during end-joining. The former stems from the inherent inability of the replication machinery to fully duplicate linear templates. Skip to Main Content.