Article
Cell Biology
Artem A. Artykov, Anne Yagolovich, Dmitry A. Dolgikh, Mikhail P. Kirpichnikov, Daria B. Trushina, Marine E. Gasparian
Summary: TRAIL induces apoptosis through DR4 and DR5 on cell surface. Death receptors are rapidly internalized upon ligand stimulation and slowly return to plasma membrane after ligand is eliminated. Inhibition of receptor endocytosis sensitizes resistant cells to TRAIL and increases its cytotoxic activity against sensitive cells.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Yana Vladimirovna Lomovskaya, Margarita Igorevna Kobyakova, Anatoly Sergeevich Senotov, Alexey Igorevich Lomovsky, Vladislav Valentinovich Minaychev, Irina Sergeevna Fadeeva, Daria Yuryevna Shtatnova, Kirill Sergeevich Krasnov, Alena Igorevna Zvyagina, Vladimir Semenovich Akatov, Roman Sergeevich Fadeev
Summary: The resistance of leukemic cells to TRAIL-induced apoptosis is a major challenge in the treatment of leukemia. In this study, researchers discovered that human acute myeloid leukemia cells, when subjected to high-density culture conditions, displayed a macrophage-like phenotype and increased resistance to TRAIL-induced cell death. This resistance can be attributed to a decrease in the expression of death receptors DR4 and DR5 on the leukemic cells. The findings suggest that stress conditions in high-density cell cultures may contribute to tumor progression by promoting TRAIL resistance.
Article
Biochemistry & Molecular Biology
Brenda Janice Sanchez, Souad Mubaid, Sandrine Busque, Yossef Lopez de los Santos, Kholoud Ashour, Jason Sadek, Xian Jin Lian, Shahryar Khattak, Sergio Di Marco, Imed-Eddine Gallouzi
Summary: mRNA stability is crucial for cell function and fate, and this study identifies YB1 as a critical partner of HuR in stabilizing mRNA and promoting myogenesis. HuR and YB1 form a complex that binds to common mRNA targets, particularly those with a U-rich consensus motif in their 3' UTR. This finding highlights the complexity of the mRNA stability mechanism and its importance in cellular processes.
NUCLEIC ACIDS RESEARCH
(2023)
Article
Multidisciplinary Sciences
Jeremy C. Burton, Jennifer Okalova, Neil J. Grimsey
Summary: In this study, the spatiotemporal dynamics of p38 activity were investigated using targeted fluorescence resonance energy transfer (FRET) p38 activity biosensors. The results showed that p38 activation through the MKK3/6 pathway exhibited enhanced activity in the nucleus, while p38 activation via the thrombin-mediated PAR1 pathway showed increased activity in the endosome and cytosol, limiting nuclear p38 activity.
SCIENTIFIC REPORTS
(2023)
Article
Cell Biology
Ya Lomovskaya, M. Kobyakova, A. S. Senotov, I. S. Fadeeva, A. Lomovsky, K. S. Krasnov, D. Yu Shtatnova, V. S. Akatov, R. S. Fadeev
Summary: The study found that induction of myeloid differentiation in leukemia cells can increase their resistance to TRAIL-induced death, but certain substances can suppress this resistance and improve treatment effectiveness.
BIOLOGICHESKIE MEMBRANY
(2022)
Article
Cell Biology
Ya. V. Lomovskaya, M. I. Kobyakova, A. S. Senotov, I. S. Fadeeva, A. I. Lomovsky, K. S. Krasnov, D. Yu. Shtatnova, V. S. Akatov, R. S. Fadeev
Summary: The study revealed that human leukemia cells THP-1, HL-60, and K562 developed resistance to TRAIL-induced death in vitro due to myeloid differentiation induced by exogenous factors, which led to reduced expression of DR4 and DR5 receptors on cell surface. Furthermore, substances such as ONC 201, tunicamycin, and SAHA, which can increase DR5 expression in leukemic cells, were found to suppress TRAIL resistance induced by differentiation factors. These findings are significant for the development of drugs and strategies to improve the treatment of myeloid leukemia.
BIOCHEMISTRY MOSCOW SUPPLEMENT SERIES A-MEMBRANE AND CELL BIOLOGY
(2023)
Article
Cell Biology
R. S. Fadeev, N. V. Dolgikh, A. V. Chekanov, A. S. Senotov, K. S. Krasnov, M. I. Kobyakova, Ya. V. Lomovskaya, I. S. Fadeeva, V. S. Akatov
Summary: The TNF alpha Related Apoptosis Inducing Ligand (TRAIL) cytokine is of interest for developing targeted antitumor drugs. Previous studies have shown that A-431 cells develop reversible resistance to TRAIL-induced apoptosis under confluent culture conditions. In this study, we found that the increased resistance is associated with reduced expression of pro-apoptotic receptors DR4 and DR5, as well as the absence of anti-apoptotic receptors DcR1 and DcR2 on the cell surface. Decreased representation of DR4 and DR5 receptors is accompanied by a lack of activation of proapoptotic protein Bid and effector caspase 3, leading to increased TRAIL resistance. These findings suggest that the reversible increase in resistance of A-431 cells to TRAIL-induced apoptosis in confluent cultures is caused by a decrease in the expression of DR4 and DR5 receptors on the cell surface.
BIOLOGICHESKIE MEMBRANY
(2023)
Article
Cell Biology
R. S. Fadeev, N. V. Dolgikh, A. V. Chekanov, A. S. Senotov, K. S. Krasnov, M. I. Kobyakova, Ya. V. Lomovskaya, I. S. Fadeeva, V. S. Akatov
Summary: In this study, we found that the increased resistance of A-431 cells to TRAIL-induced apoptosis in confluent cultures is associated with reduced expression of pro-apoptotic receptors DR4 and DR5, as well as the absence of anti-apoptotic receptors DcR1 and DcR2 on the cell surface. The decreased representation of DR4 and DR5 receptors is accompanied by a lack of activation of the pro-apoptotic protein Bid and effector caspase 3 under the action of recombinant protein izTRAIL, leading to an increase in TRAIL resistance. These results suggest that the reversible increase in TRAIL resistance in A-431 cells is caused by a decrease in the expression of DR4 and DR5 receptors on the cell surface.
BIOCHEMISTRY MOSCOW SUPPLEMENT SERIES A-MEMBRANE AND CELL BIOLOGY
(2023)
Review
Endocrinology & Metabolism
S. Kahraman, C. Aydin, G. O. Elpek, E. Dirice, A. D. Sanlioglu
JOURNAL OF DIABETES RESEARCH
(2015)
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Clinical Neurology
Irem Kanatli, Bahar Akkaya, Hilmi Uysal, Sevim Kahraman, Ahter Dilsad Sanlioglu
NEUROMUSCULAR DISORDERS
(2017)
Article
Biochemistry & Molecular Biology
Hale M. Tasyurek, Yunus E. Eksi, Ahter D. Sanlioglu, Hasan A. Altunbas, Mustafa K. Balci, Thomas S. Griffith, Salih Sanlioglu
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Oncology
Cigdem Aydin, Ahter D. Sanlioglu, Atil Bisgin, Burcak Yoldas, Levent Dertsiz, Bahri Karacay, Thomas S. Griffith, Salih Sanlioglu
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Endocrinology & Metabolism
Sevim Kahraman, Ercument Dirice, Fatma Z. Hapil, Mustafa G. Ertosun, Saffet Ozturk, Thomas S. Griffith, Salih Sanlioglu, Ahter D. Sanlioglu
DIABETES-METABOLISM RESEARCH AND REVIEWS
(2011)
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Endocrinology & Metabolism
Ercument Dirice, Sevim Kahraman, Gulsum Ozlem Elpek, Cigdem Aydin, Mustafa Kemal Balci, Abdulkadir Omer, Salih Sanlioglu, Ahter Dilsad Sanlioglu
EXPERIMENTAL DIABETES RESEARCH
(2011)
Review
Biochemistry & Molecular Biology
Ahter D. Sanlioglu, Hasan Ali Altunbas, Mustafa Kemal Balci, Thomas S. Griffith, Salih Sanlioglu
EXPERT REVIEWS IN MOLECULAR MEDICINE
(2012)
Article
Oncology
Emel Sahin, Mehmet Sahin, Ahter Dilsad Sanlioglu, Saadet Gumuslu
INTERNATIONAL JOURNAL OF HYPERTHERMIA
(2011)
Review
Endocrinology & Metabolism
Ahter D. Sanlioglu, Bahri Karacay, Mustafa Kemal Balci, Thomas S. Griffith, Salih Sanlioglu
JOURNAL OF MOLECULAR ENDOCRINOLOGY
(2012)
Article
Radiology, Nuclear Medicine & Medical Imaging
Sevim Kahraman, Ercument Dirice, Ahter Dilsad Sanlioglu, Burcak Yoldas, Huseyin Bagci, Metin Erkilic, Thomas S. Griffith, Salih Sanlioglu
MOLECULAR IMAGING AND BIOLOGY
(2010)
Article
Urology & Nephrology
Ismail Turker Koksal, Ahter Dilsad Sanlioglu, Omer Kutlu, Salih Sanlioglu
UROLOGIA INTERNATIONALIS
(2010)
Review
Endocrinology & Metabolism
Ahter D. Sanlioglu, Hasan Ali Altunbas, Mustafa Kemal Balci, Thomas S. Griffith, Salih Sanlioglu
Article
Medicine, Research & Experimental
Hasan Onur Arik, Arzu Didem Yalcin, Saadet Gumuslu, Gizem Esra Genc, Adil Turan, Ahter Dilsad Sanlioglu
MEDICAL SCIENCE MONITOR
(2013)
Article
Oncology
Mujgan Timur, Aysegul Cort, Evrim Ozdemir, Sureyya Bilmen Sarikcioglu, Salih Sanlioglu, Ahter Dilsad Sanlioglu, Tomris Ozben
ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
(2015)