Results 81 to 90 of about 510,810 (316)

Transcriptional profiling of circulating extracellular vesicles from prebiopsy prostate cancer patients

Molecular Oncology, EarlyView.
RNA profiling of circulating extracellular vesicles (EVs) from blood samples of men undergoing prostate biopsy identifies transcripts associated with clinically significant prostate cancer. Integrative analysis with public tumor datasets links EV‐derived gene signatures to tumor stage and progression‐free survival, highlighting CASP3, XRCC2, and RIT1 ...
Stefan Werner, Pierre Tennstedt, Randi C. Pose, Christian Müller, Katharina Besler, Svenja Schneegans, Malik Alawi, Marie C. Roesch, Sven Peine, Desiree Bonci, Joanna Budna‐Tukan, Evi Lianidou, Catherine Alix‐Panabières, Derya Tilki, Klaus Pantel   +14 more
wiley   +1 more source

Species-Specific Contribution of the Four C-Terminal Amino Acids of Influenza A Virus NS1 Protein to Virulence [PDF]

, 2010
Large-scale sequence analyses of influenza viruses revealed that nonstructural 1 (NS1) proteins from avian influenza viruses have a conserved C-terminal ESEV amino acid motif, while NS1 proteins from typical human influenza viruses have a C-terminal RSKV
Loupias, Josiane, Lacroux, Caroline, Peralta, Brigitte, Soubies, S. M., Soubiès, Sébastien, Loupias, Josyane, Costes, Pierrette, Guérin, Jean-Luc, Volmer, C., Volmer, Christelle, Croville, Guillaume, Soubies, Sebastien Mathieu, Volmer, Romain   +12 more
core   +1 more source

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

Protein-protein interactions leading to recruitment of the host DNA sliding clamp by the hyperthermophilic Sulfolobus islandicus rod- shaped virus 2 [PDF]

, 2014
Viruses infecting hyperthermophilic archaea typically do not encode DNA polymerases, raising questions regarding their genome replication. Here, using a yeast two-hybrid approach, we have assessed interactions between proteins of Sulfolobus islandicus ...
Gardner, A.F., Bell, S.D., Krupovic, M., Prangishvili, D., White, M.F.   +4 more
core   +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

Inhibition of the foot-and-mouth disease virus subgenomic replicon by RNA aptamers. [PDF]

, 2014
We have previously documented the inhibitory activity of RNA aptamers to the RNA-dependent RNA polymerase of foot-and-mouth disease virus (3D(pol)). Here we report their modification and use with a subgenomic replicon incorporating GFP (pGFP-PAC replicon)
Forrest, S, Lear, Z, Ryan, M., Herod, M, Forrest, S., Ryan, M, Stonehouse, N.J., Rowlands, DJ, Herod, M.R., Stonehouse, NJ, Lear, Z., Rowlands, D.J.   +11 more
core   +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

Chikungunya virus nonstructural protein 2 inhibits type I/II interferon-stimulated JAK-STAT signaling [PDF]

, 2010
Chikungunya virus (CHIKV) is an emerging human pathogen transmitted by mosquitoes. Like that of other alphaviruses, CHIKV replication causes general host shutoff, leading to severe cytopathicity in mammalian cells, and inhibits the ability of infected ...
Ligtenberg, M., Suhrbier, A., Corinne Geertsema, Esther Schnettler, Fros, J., Just M. Vlak, Maarten Ligtenberg, Geertsema, C., Suhrbier, Andreas, Wen Jun Liu, Natalie A. Prow, Vlak, J.M., Dana L. Vanlandingham, Ligtenberg, Maarten, Khromykh, Alexander A., Jelke J. Fros, Vanlandingham, D.L., Vlak, Just M., Schnettler, E., Fros, J.J., Gorben P. Pijlman, Pijlman, G.P., Liu, W.J., Khromykh, A.A., Prow, A., Fros, Jelke J., Vanlandingham, Dana L., Liu, Wen Jun, Geertsema, Corinne, Prow, Natalie A., Alexander A. Khromykh, Schnettler, Esther, Pijlman, Gorben P., Andreas Suhrbier, Prow, N.A.   +34 more
core   +1 more source

Riboswitching on RNA virus replication [PDF]

Proceedings of the National Academy of Sciences, 2007
Positive-strand RNA viruses direct different virus-specific processes during their infection of host cells. Fundamental events such as viral RNA genome replication are controlled by viral regulatory RNA elements (REs). Here, we have investigated the possibility of specifically modulating the action of a viral RE using RNA aptamer technology.
Sheng, Wang, K Andrew, White
openaire   +2 more sources

ZW4864‐mediated inhibition of the β‐catenin/BCL9/BCL9L complex reveals therapeutic potential in bladder cancer

Molecular Oncology, EarlyView.
BCL9 and BCL9L drive bladder cancer progression by enhancing β‐catenin signaling, promoting proliferation, migration, invasion, and organoid growth. Genetic depletion of BCL9(L) suppresses malignant phenotypes, while pharmacological disruption of the β‐catenin/BCL9(L) complex with ZW4864 inhibits canonical Wnt signaling and tumor‐associated cellular ...
Roland Kotolloshi, Mandy Berndt‐Paetz, Eileen Lerner, Gregoire Najjar, Anca Azoitei, Krishna Pal Singh, Shailendra Kumar Gupta, Olaf Wolkenhauer, Cagatay Günes, Otmar Huber, Marc‐Oliver Grimm, Daniel Steinbach   +11 more
wiley   +1 more source