Results 61 to 70 of about 32,945 (258)

Key residues of Bacillus thuringiensis Cry2Ab for oligomerization and pore-formation activity

AMB Express, 2021
As a pore-forming toxin, activation, oligomerization and pore-formation were both required for the mode of action of Cry toxins. Previous results revealed that the helices α4–α5 of Domain I were involved in the oligomerization of Cry2Ab, however, the key
Zhi-Zhen Pan, Lian Xu, Bo Liu, Qing-Xi Chen, Yu-Jing Zhu   +4 more
doaj   +1 more source

The Pore-forming Toxin Proaerolysin Is Activated by Furin [PDF]

Journal of Biological Chemistry, 1998
Aerolysin is secreted as an inactive dimeric precursor by the bacterium Aeromonas hydrophila. Proteolytic cleavage within a mobile loop near the C terminus of the protoxin is required for oligomerization and channel formation. This loop contains the sequence KVRRAR432, which should be recognized by mammalian proprotein convertases such as furin, PACE4,
Abrami, Laurence, Fivaz, Marc, Decroly, Etienne, Seidah, Nabil, Jean, François, Thomas, Gary, Leppla, Stephen H., Buckley, Thomas, Van Der Goot Grunberg, Françoise G.   +8 more
openaire   +3 more sources

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

Molecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak, Bodee Nutho, Worawat Wattanathana, Narumon Phaonakrop, Bunnatut Panasawatwong, Katharina Erlenbach‐Wuensch, Sittiruk Roytrakul, Regine Schneider‐Stock, Pithi Chanvorachote   +8 more
wiley   +1 more source

Glycosylated LGALS3BP is highly secreted by bladder cancer cells and represents a novel urinary disease biomarker

Molecular Oncology, EarlyView.
Urinary LGALS3BP is elevated in bladder cancer patients compared to healthy controls as detected by the 1959 antibody–based ELISA. The antibody shows enhanced reactivity to the high‐mannose glycosylated variant secreted by cancer cells treated with kifunensine (KIF).
Asia Pece, Giulio Lovato, Ilaria Cela, Arianna Mercatelli, Benedetta Ferro, Jussi Nikkola, Sara Pagotto, Tommaso Grottola, Vincenzo De Laurenzi, Rossella Cicchetti, Antonio Marchetti, Luigi Schips, Rossano Lattanzio, Stefano Iacobelli, Emily Capone, Peter Black, Mads Daugaard, Michele Marchioni, Gianluca Sala   +18 more
wiley   +1 more source

CDK11 inhibition induces cytoplasmic p21WAF1 splice variant by p53 stabilisation and SF3B1 inactivation

Molecular Oncology, EarlyView.
CDK11 inhibition stabilises the tumour suppressor p53 and triggers the production of an alternative p21WAF1 splice variant p21L, through the inactivation of the spliceosomal protein SF3B1. Unlike the canonical p21WAF1 protein, p21L is localised in the cytoplasm and has reduced cell cycle‐blocking activity.
Radovan Krejcir, Lukasz Arcimowicz, Lucia Martinkova, Vaclav Hrabal, Filip Zavadil Kokas, Tomas Henek, Martina Kucerikova, Ondrej Bonczek, Pavlina Zatloukalova, Lenka Hernychova, Philip J. Coates, Borivoj Vojtesek, David P. Lane   +12 more
wiley   +1 more source

Improving PARP inhibitor efficacy in bladder cancer without genetic BRCAness by combination with PLX51107

Molecular Oncology, EarlyView.
Clinical trials on PARP inhibitors in urothelial carcinoma (UC) showed limited efficacy and a lack of predictive biomarkers. We propose SLFN5, SLFN11, and OAS1 as UC‐specific response predictors. We suggest Talazoparib as the better PARP inhibitor for UC than Olaparib.
Jutta Schmitz, Anna L. Bartkowiak, Michael Rose, Nora Kolks, Patrick Petzsch, Vandana Solanki, Anne Stoffel, Bianca Faßbender, Leandra Lepping, Julka Volkamer, Karl Köhrer, Marc Seifert, Tokameh Mahmoudi, Tahlita C. M. Zuiverloon, Günter Niegisch, Michèle J. Hoffmann   +15 more
wiley   +1 more source

Apicomplexan Pore-Forming Toxins

Annual Review of Microbiology
Pore-forming toxins (PFTs) are released by one cell to directly inflict damage on another cell. Hosts use PFTs, including members of the membrane attack complex/perforin protein family, to fight infections and cancer, while bacteria and parasites deploy PFTs to promote infection.
openaire   +2 more sources

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

Molecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto, Nicolò Gualandi, Ylenia Cortolezzis, Raffaella Picco, Monica Colitti, Francesca D'Este, Mariachiara Gani, Wayne W. Hancock, Giovanni Terrosu, Cristina Degrassi, Francesca Agostini, Claudio Brancolini, Luigi E. Xodo, Eros Di Giorgio   +13 more
wiley   +1 more source

Dual targeting of RET and SRC synergizes in RET fusion‐positive cancer cells

Molecular Oncology, EarlyView.
Despite the strong activity of selective RET tyrosine kinase inhibitors (TKIs), resistance of RET fusion‐positive (RET+) lung cancer and thyroid cancer frequently occurs and is mainly driven by RET‐independent bypass mechanisms. Son et al. show that SRC TKIs significantly inhibit PAK and AKT survival signaling and enhance the efficacy of RET TKIs in ...
Juhyeon Son, Lily L. Remsing Rix, Bin Fang, Eric A. Welsh, Nicole V. Bremer, Valentina Foglizzo, Paola Roa, Nickole Sigcha‐Coello, Yi Liao, Eric B. Haura, Alexander Drilon, John M. Koomen, Emiliano Cocco, Uwe Rix   +13 more
wiley   +1 more source

Potential therapeutic targeting of BKCa channels in glioblastoma treatment

Molecular Oncology, EarlyView.
This review summarizes current insights into the role of BKCa and mitoBKCa channels in glioblastoma biology, their potential classification as oncochannels, and the emerging pharmacological strategies targeting these channels, emphasizing the translational challenges in developing BKCa‐directed therapies for glioblastoma treatment.
Kamila Maliszewska‐Olejniczak, Karolina Pytlak, Sandra Jaworowska, Bogusz Kulawiak, Piotr Bednarczyk   +4 more
wiley   +1 more source