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6 results on '"Golforoush, Pelin Arabacilar"'

1. Advancements in risk stratification and management strategies in primary cardiovascular prevention

Author

Barkas, Fotios, Sener, Yusuf Ziya, Golforoush, Pelin Arabacilar, Kheirkhah, Azin, Rodriguez-Sanchez, Elena, Novak, Jan, Apellaniz-Ruiz, Maria, Akyea, Ralph Kwame, Bianconi, Vanessa, Ceasovschih, Alexandr, Chee, Ying Jie, Cherska, Mariia, Chora, Joana Rita, D'Oria, Mario, Demikhova, Nadiia, Kocyigit Burunkaya, Duygu, Rimbert, Antoine, Macchi, Chiara, Rathod, Krishnaraj, Roth, Lynn, Sukhorukov, Vasily, Stoica, Svetlana, Scicali, Roberto, Storozhenko, Tatyana, Uzokov, Jamol, Lupo, Maria Giovanna, van der Vorst, Emiel P.C., and Porsch, Florentina

Published
2024
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2. MAP4K4 Inhibition Promotes Survival of Human Stem Cell-Derived Cardiomyocytes and Reduces Infarct Size In Vivo

Author

Fiedler, Lorna R., Chapman, Kathryn, Xie, Min, Maifoshie, Evie, Jenkins, Micaela, Golforoush, Pelin Arabacilar, Bellahcene, Mohamed, Noseda, Michela, Faust, Dörte, Jarvis, Ashley, Newton, Gary, Paiva, Marta Abreu, Harada, Mutsuo, Stuckey, Daniel J., Song, Weihua, Habib, Josef, Narasimhan, Priyanka, Aqil, Rehan, Sanmugalingam, Devika, Yan, Robert, Pavanello, Lorenzo, Sano, Motoaki, Wang, Sam C., Sampson, Robert D., Kanayaganam, Sunthar, Taffet, George E., Michael, Lloyd H., Entman, Mark L., Tan, Tse-Hua, Harding, Sian E., Low, Caroline M.R., Tralau-Stewart, Catherine, Perrior, Trevor, and Schneider, Michael D.

Published
2019
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4. MAP4K4 Inhibition Promotes Survival of Human Stem Cell-Derived Cardiomyocytes and Reduces Infarct Size In Vivo

Author

Fiedler, Lorna R., primary, Chapman, Kathryn, additional, Xie, Min, additional, Maifoshie, Evie, additional, Jenkins, Micaela, additional, Golforoush, Pelin Arabacilar, additional, Bellahcene, Mohamed, additional, Noseda, Michela, additional, Faust, Dörte, additional, Jarvis, Ashley, additional, Newton, Gary, additional, Paiva, Marta Abreu, additional, Harada, Mutsuo, additional, Stuckey, Daniel J., additional, Song, Weihua, additional, Habib, Josef, additional, Narasimhan, Priyanka, additional, Aqil, Rehan, additional, Sanmugalingam, Devika, additional, Yan, Robert, additional, Pavanello, Lorenzo, additional, Sano, Motoaki, additional, Wang, Sam C., additional, Sampson, Robert D., additional, Kanayaganam, Sunthar, additional, Taffet, George E., additional, Michael, Lloyd H., additional, Entman, Mark L., additional, Tan, Tse-Hua, additional, Harding, Sian E., additional, Low, Caroline M.R., additional, Tralau-Stewart, Catherine, additional, Perrior, Trevor, additional, and Schneider, Michael D., additional

Published
2020
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5. The TAB1-p38α complex aggravates myocardial injury and can be targeted by small molecules

Author

De Nicola, Gian F., Bassi, Rekha, Nichols, Charlie, Fernandez-Caggiano, Mariana, Golforoush, Pelin Arabacilar, Thapa, Dibesh, Anderson, Rhys, Martin, Eva Denise, Verma, Sharwari, Kleinjung, Jens, Laing, Adam, Hutchinson, Jonathan P., Eaton, Philip, Clark, James, and Marber, Michael S.

Subjects
Pharmacology, Protein kinases, Cardiology, Therapeutics, Structural biology
Abstract

Inhibiting MAPK14 (p38α) diminishes cardiac damage in myocardial ischemia. During myocardial ischemia, p38α interacts with TAB1, a scaffold protein, which promotes p38α autoactivation; active p38α (pp38α) then transphosphorylates TAB1. Previously, we solved the X-ray structure of the p38α-TAB1 (residues 384-412) complex. Here, we further characterize the interaction by solving the structure of the pp38α-TAB1 (residues 1-438) complex in the active state. Based on this information, we created a global knock-in (KI) mouse with substitution of 4 residues on TAB1 that we show are required for docking onto p38α. Whereas ablating p38α or TAB1 resulted in early embryonal lethality, the TAB1-KI mice were viable and had no appreciable alteration in their lymphocyte repertoire or myocardial transcriptional profile; nonetheless, following in vivo regional myocardial ischemia, infarction volume was significantly reduced and the transphosphorylation of TAB1 was disabled. Unexpectedly, the activation of myocardial p38α during ischemia was only mildly attenuated in TAB1-KI hearts. We also identified a group of fragments able to disrupt the interaction between p38α and TAB1. We conclude that the interaction between the 2 proteins can be targeted with small molecules. The data reveal that it is possible to selectively inhibit signaling downstream of p38α to attenuate ischemic injury.

Published
2018
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6. The TAB1-p38α complex aggravates myocardial injury and can be targeted by small molecules

Author

De Nicola, Gian F., primary, Bassi, Rekha, additional, Nichols, Charlie, additional, Fernandez-Caggiano, Mariana, additional, Golforoush, Pelin Arabacilar, additional, Thapa, Dibesh, additional, Anderson, Rhys, additional, Martin, Eva Denise, additional, Verma, Sharwari, additional, Kleinjung, Jens, additional, Laing, Adam, additional, Hutchinson, Jonathan P., additional, Eaton, Philip, additional, Clark, James, additional, and Marber, Michael S., additional

Published
2018
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