Kökrek, Emel

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Name Variants
KÖKREK, Emel
Kokrek,E.
K.,Emel
EMEL KÖKREK
Emel Kökrek
Kökrek, E.
KÖKREK, EMEL
Emel, Kokrek
Emel KÖKREK
Kökrek, Emel
K., Emel
Kokrek, Emel
Kökrek,E.
Kokrek,Emel
Kökrek, EMEL
E. Kökrek
Job Title
Araş. Gör.
Email Address
emel.kokrek@khas.edu.tr
Main Affiliation
Molecular Biology and Genetics
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Website
ORCID ID
0000-0002-8379-9617
Scopus Author ID
Turkish CoHE Profile ID
Google Scholar ID
WoS Researcher ID
DBD-1060-2022
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    Article
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    Distinct Deregulation Trends of Transcriptional Protein Complexes in Aging Naive T Cells
    (Oxford Univ Press, 2024) Kökrek, Emel; Pir, Pinar
    The impact of aging on T cell subsets, specifically CD4+ and CD8+ T cells, leading to immune system dysfunction has been the focus of scientific investigation due to its potential to reverse age-associated deterioration. Transcriptomic and epigenomic studies have identified the primary regulators in T cell aging. However, comprehending the underlying dynamic mechanisms requires studying these proteins with their interactors. Here, we integrated single-cell RNA sequencing data of naive CD4+ and CD8+ T cells obtained from 3 different age groups with protein-protein and domain-domain interaction networks to predict and compare the transcriptional protein complexes and identify their capacity to explain age-associated variances. Our novel approach revealed significant effects of aging on the repertoire of complexes, which remains unchanged in naive CD4+ T cells, while in naive CD8+ T cells, it diminishes. In both cell types, there was major deregulation of complexes with the same composition, involving a range of transcription factors. This aging-associated deregulation is characterized by a specific set of protein complexes in naive CD4+ T cells, but this pattern is not observed in naive CD8+ T cells. SMAD3 and BCL11A complexes emerge as key markers in defining a trajectory in aging naive CD4+ T cells. These complexes can accurately distinguish between 3 different age groups, indicating their potential as targets. The direct link between SMAD3 and FOS complexes whose regulatory role has been previously implicated in aging and MBD3 as the novel key link between SMAD3 and BCL11A complexes implicates a coordinated mechanism in age-associated deregulation.