Results 101 to 110 of about 1,209,228 (250)

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

Molecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source

Antimicrobial peptides and complement in neonatal hypoxia-ischemia induced brain damage [PDF]

, 2015
Hypoxic-ischemic encephalopathy (HIE) is a clinical condition in the neonate, resulting from oxygen deprivation around the time of birth. HIE affects 1-5/1000 live births worldwide and is associated with the development of neurological deficits ...
Rocha-Ferreira, E, Eridan Rocha-Ferreira, Eridan eRocha-Ferreira, Mariya eHristova, Hristova, M, Mariya Hristova   +5 more
core   +1 more source

Current status and perspectives of hematopoietic cell transplantation in patients with paroxysmal nocturnal hemoglobinuria

Frontiers in Immunology
BackgroundParoxysmal nocturnal hemoglobinuria (PNH) is a rare complement-driven acquired hemolytic anemia with specific presentations of hemoglobinuria, abdominal pain, fatigue, and thrombosis.ObjectiveTo review the current therapeutic strategies for PNH,
Marek Ussowicz, Dawid Przystupski, Patrycja Mensah-Glanowska, Agnieszka Piekarska   +3 more
doaj   +1 more source

Peptide Inhibitor of Complement C1 (PIC1) Rapidly Inhibits Complement Activation after Intravascular Injection in Rats.

PLoS ONE, 2015
The complement system has been increasingly recognized to play a pivotal role in a variety of inflammatory and autoimmune diseases. Consequently, therapeutic modulators of the classical, lectin and alternative pathways of the complement system are ...
Julia A Sharp, Pamela S Hair, Haree K Pallera, Parvathi S Kumar, Clifford T Mauriello, Julius O Nyalwidhe, Cody A Phelps, Dalnam Park, Nicole M Thielens, Stephen M Pascal, Waldon Chen, Diane M Duffy, Frank A Lattanzio, Kenji M Cunnion, Neel K Krishna   +14 more
doaj   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

Molecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder, Klaas de Lint, Hồ Mỹ Phúc Võ, Mariana M. Góis, Rosalie A. Kampen, Marta San Martin Alonso, Ilse Nootenboom, Veronica Garzero, Tiemen J. Wendel, Rob M. F. Wolthuis, Sylvie M. Noordermeer   +10 more
wiley   +1 more source

A novel quinazolinone insulin receptor inhibitor and its synergy with an EGFR inhibitor in glucose‐driven glioblastoma

Molecular Oncology, EarlyView.
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka, Wioleta Cieślik, Wojciech Płaziński, Katarzyna Stępnik, Anna Boguszewska‐Czubara, Elżbieta Kot, Robert Musioł, Mateusz Jasica, Anna Mrozek‐Wilczkiewicz, Katarzyna Malarz   +9 more
wiley   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

Molecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu, Nicolas J. Niklaus, Anna M. Schläfli, Igor Tokarchuk, Magali Humbert, Federico La Manna, Bich Vu, David Maul, Ramin Radpour, Marianna Kruithof‐de Julio, Inti Zlobec, Jörn Dengjel, Bruce E. Torbett, Mario P. Tschan   +13 more
wiley   +1 more source

Advancements in complement inhibition for PNH and primary complement–mediated thrombotic microangiopathy

Blood Advances
: Paroxysmal nocturnal hemoglobinuria (PNH) and primary complement–mediated thrombotic microangiopathy, also known as atypical hemolytic uremic syndrome (aHUS), are hematologic disorders characterized by dysregulation of the complement system leading to ...
Thalia Padilla Kelley, Hannah King, Aditya Malhotra, Thomas G. DeLoughery, Kylee Martens, Joseph J. Shatzel   +5 more
doaj   +1 more source

Loss of proton‐sensing TDAG8 increases tumor progression in mouse models of colon cancer

Molecular Oncology, EarlyView.
Loss of the pH‐sensing receptor TDAG8 accelerates colorectal cancer progression in mice. Animals lacking TDAG8 expression had increased tumor growth, DNA damage, and recruitment of tumor‐associated immune cells, including macrophages, neutrophils, and monocytes.
Ermanno Malagola, Yasmine Illi, Anna Bircher, Marijn Wilmink, Rachele F. Malagutti, Solenn Ottié, Cordelia Schuler, Pedro A. Ruiz, Cheryl de Vallière, Klaus Seuwen, Gerhard Rogler, Martin Hausmann   +11 more
wiley   +1 more source

Epigenetic heterogeneity and plasticity in therapy‐induced tumor states through single‐cell multi‐omics

Molecular Oncology, EarlyView.
Single‐cell multi‐omics reveals epigenetic heterogeneity across therapy‐adaptive tumor states, including quiescent/dormant, drug‐tolerant persister, and EMT‐like phenotypes. By linking regulatory features with state‐associated biomarkers, these approaches inform biomarker‐guided therapeutic strategies for evolving tumors.
Hee Jung Kim, Hwiyeong Lee, Jin Hong, Daechan Park   +3 more
wiley   +1 more source