Results 81 to 90 of about 247,050 (333)

Tonic signaling of the B‐cell antigen‐specific receptor is a common functional hallmark in chronic lymphocytic leukemia cell phosphoproteomes at early disease stages

Molecular Oncology, EarlyView.
B‐cell chronic lymphocytic leukemia (B‐CLL) and monoclonal B‐cell lymphocytosis (MBL) show altered proteomes and phosphoproteomes, analyzed using mass spectrometry, protein microarrays, and western blotting. Identifying 2970 proteins and 316 phosphoproteins, including 55 novel phosphopeptides, we reveal BCR and NF‐kβ/STAT3 signaling in disease ...
Paula Díez, Pablo Juanes‐Velasco, Marina L. García‐Vaquero, Conrad Droste, Alicia Landeira‐Viñuela, Miguel Alcoceba, Helena Fidalgo‐Gómez, Sara Misiego‐Herrero, Almudena Navarro‐Bailón, Mónica Baile, José M. Bastida, Jose Manuel Sanchez‐Santos, Rafael Góngora, Julia Almeida, Marcos Gonzalez‐Diaz, Alberto Orfao, Javier De Las Rivas, Manuel Fuentes   +17 more
wiley   +1 more source

Inhibition of the classical pathway of the complement cascade prevents early dendritic and synaptic degeneration in glaucoma

Molecular Neurodegeneration, 2016
Glaucoma is a complex, multifactorial disease characterised by the loss of retinal ganglion cells and their axons leading to a decrease in visual function. The earliest events that damage retinal ganglion cells in glaucoma are currently unknown.
Pete A. Williams, James R. Tribble, Keating W. Pepper, S. D. Cross, B. Morgan, J. Morgan, S. John, S. John, G. Howell   +8 more
semanticscholar   +1 more source

Blood platelets activate the classical pathway of human complement [PDF]

Journal of Thrombosis and Haemostasis, 2006
Activation of the complement system plays a key role in inflammation associated with vascular injury. Recently, platelet P-selectin was shown to activate C3 via the alternative pathway of human complement. As platelets also posses binding sites for C1q, the recognition unit of the classical complement pathway, the present study examined classical ...
Ellinor I.B. Peerschke, Berhane Ghebrehiwet, Wei Yin, S. E. Grigg   +3 more
openaire   +3 more sources

Simultaneous inhibition of TRIM24 and TRIM28 sensitises prostate cancer cells to antiandrogen therapy, decreasing VEGF signalling and angiogenesis

Molecular Oncology, EarlyView.
TRIM24 and TRIM28 are androgen receptor (AR) coregulators which exhibit increased expression with cancer progression. Both TRIM24 and TRIM28 combine to influence the response of castrate‐resistant prostate cancer (CRPC) cells to AR inhibitors by mediating AR signalling, regulation of MYC and upregulating VEGF to promote angiogenesis. Castrate‐resistant
Damien A. Leach, Nilesh Chatterjee, Kellie Spahr, Gilberto Serrano de Almeida, Anabel Varela‐Carver, Taimur T. Shah, Mathias Winkler, Hashim U. Ahmed, Charlotte L. Bevan   +8 more
wiley   +1 more source

Integrative miRNOMe profiling reveals the miR‐195‐5p–CHEK1 axis and its impact on luminal breast cancer outcomes

Molecular Oncology, EarlyView.
In luminal (ER+) breast carcinoma (BC), miRNA profiling identified miR‐195‐5p as a key regulator of proliferation that targets CHEK1, CDC25A, and CCNE1. High CHEK1 expression correlates with worse relapse‐free survival after chemotherapy, especially in patients with luminal A subtype.
Veronika Boušková, Marie Ehrlichová, Alžběta Spálenková, Ivona Krus, Simona Šůsová, Viktor Hlaváč, Vlasta Němcová, Renata Koževnikovová, Markéta Trnková, David Vrána, Jiří Gatěk, Kateřina Kopečková, Marcela Mrhalová, Soňa Měšťáková, Pavel Souček   +14 more
wiley   +1 more source

Borrelia valaisiana resist complement-mediated killing independently of the recruitment of immune regulators and inactivation of complement components [PDF]

, 2013
Spirochetes belonging to the Borrelia (B.) burgdorferi sensu lato complex differ in their resistance to complement-mediated killing, particularly in regard to human serum.
A Alitalo, A Alitalo, A Alitalo, A Seling, AC Steere, AM Blom, Andreas Klos, AP van Dam, B Stevenson, C Hammerschmidt, C Siegel, C Siegel, Christine Skerka, Claudia Hammerschmidt, CS Brooks, Dania Richter, E Diza, F Strle, Franz-Rainer Matuschka, H Jiang, H Michel, J Hellwage, J Pietikainen, J Potempa, Jasmin Schwab, JD Lambris, JV McDowell, K Hartmann, K Haupt, K Kurtenbach, K Kurtenbach, K Saito, K Whaley, KM Hovis, KP Hunfeld, L Beinrohr, M Collares-Pereira, M Jusko, M Józsi, MJ Walport, MK Pangburn, MR Bhide, MR Bhide, MR Kenedy, MS Metts, N Marr, ND van Burgel, P Herzberger, P Herzberger, P Kraiczy, P Kraiczy, P Kraiczy, P Kraiczy, P Kraiczy, P Kraiczy, P Ramu, Peter F. Zipfel, Peter Kraiczy, PF Zipfel, PF Zipfel, R Dieterich, R Wallich, Reinhard Wallich, RG Discipio, RJ Ziccardi, S Breitner-Ruddock, S Grosskinsky, S Grosskinsky, S Heinen, S Kühn, SC Bock, SG Rijpkema, SH Rooijakkers, T Fujita, T Fujita, V Brade, Y Terao   +76 more
core   +6 more sources

Hypoxic Processes Induce Complement Activation via Classical Pathway in Porcine Neuroretinas

Cells, 2021
Considering the fact that many retinal diseases are yet to be cured, the pathomechanisms of these multifactorial diseases need to be investigated in more detail.
Ana M. Mueller-Buehl, Torsten Buehner, Christiane Pfarrer, Leonie Deppe, Laura Peters, Burkhard H. Dick, Stephanie C. Joachim   +6 more
doaj   +1 more source

A Computational and Experimental Study of the Regulatory Mechanisms of the Complement System [PDF]

, 2010
The complement system is key to innate immunity and its activation is necessary for the clearance of bacteria and apoptotic cells. However, insufficient or excessive complement activation will lead to immune-related diseases. It is so far unknown how the
A Krarup, A Thern, AA Korotaevskiy, AF Zadura, AM Blom, AM Blom, AM Blom, Anna M. Blom, AP Sjoberg, AP Sjoberg, B Dahlback, B Liu, B Selander, Benjamin Leong, Bing Liu, Bow Ho, C Mold, CJ Langmead, D Ricklin, D Sheskin, David Hsu, DH Anderson, DT Fearon, DT Fearon, G Koh, H Hirayama, I Gigli, I Gigli, J Gunawardena, J Scharfstein, J Zhang, Jeak Ling Ding, JH Griffin, Jing Zhang, K Berggard, KP Murphy, KP Murphy, L Marnell, L Truedsson, LM Boerger, M Bozga, M Jaeger, M Matsushita, M Okroj, MH Kaplan, MJ Walport, MJ Walport, MV Suresh, N Rawal, NA van Riel, NV Prasadarao, P. S. Thiagarajan, Pei Yi Tan, PM Ng, R Veerhuis, Rustom Antia, S Hoops, S Jha, S Ram, SR Barnum, Sunil Sethi, T Fujita, T Meri, T Nordstrom, V Kirjavainen, X Ji, Z Fishelson, Z Zi   +67 more
core   +4 more sources

Olaparib synergy screen reveals Exemestane induces replication stress in triple‐negative breast cancer

Molecular Oncology, EarlyView.
Screening 166 FDA‐approved anticancer drugs identifies the aromatase inhibitor Exemestane as a synergistic partner of PARP inhibitor Olaparib in BRCA‐proficient triple‐negative breast cancer. Exemestane induces ROS‐mediated replication stress, enhancing DNA damage and apoptosis alongside Olaparib.
Nur Aininie Yusoh, Liping Su, Suet Lin Chia, Xiaohe Tian, Haslina Ahmad, Martin R. Gill   +5 more
wiley   +1 more source

Is the Complement Protein C1q a Pro- or Anti-tumorigenic Factor? Bioinformatics Analysis Involving Human Carcinomas

Frontiers in Immunology, 2019
C1q is the first subcomponent of the classical pathway of the complement system and belongs to the C1q/Tumor Necrosis Factor superfamily. C1q can perform a diverse range of immune and non-immune functions in a complement-dependent as well as -independent
Alessandro Mangogna, Chiara Agostinis, Deborah Bonazza, Beatrice Belmonte, Paola Zacchi, Gabriella Zito, Andrea Romano, Fabrizio Zanconati, Giuseppe Ricci, Giuseppe Ricci, Uday Kishore, Roberta Bulla   +11 more
doaj   +1 more source