Results 151 to 160 of about 3,273,753 (252)

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

Molecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu, Xixi Lin, Emil Mladenov, Veronika Mladenova, Jürgen Thomale, Ali Sak, Yao Wang, Yunxuan Deng, Eleni Gkika, Martin Stuschke, George Iliakis   +10 more
wiley   +1 more source

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

Molecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

Quantum-augmented graph differential geometry enhances accuracy in protein-protein interaction prediction. [PDF]

Sci Rep
Karthick V, Alshammari FS, Jayasimman IP, Besi PR, Akgul A.   +4 more
europepmc   +1 more source

NKCC1: A key regulator of glioblastoma progression

Molecular Oncology, EarlyView.
Glioblastoma (GBM) progression is driven by disrupted chloride cotransporter homeostasis. NKCC1 is highly expressed in stem‐like, astrocytic, and progenitor cells, correlating with earlier recurrence, while overall survival remains unaffected. NKCC1 serves as a prognostic marker and potential therapeutic target, linking chloride transporter imbalance ...
Anja Thomsen, Diana Freitag, Madlen Haase, Christian Senft, Falko Schwarz, Silke Keiner   +5 more
wiley   +1 more source

Human protein-protein interaction prediction

BMC Bioinformatics, 2010
Scott Michelle S, McDowall Mark D, Barton Geoffrey J   +2 more
doaj   +1 more source

Molecular tweezer-peptide conjugates disrupt the protein-protein interaction between survivin and histone H3 essential in mitosis. [PDF]

Beilstein J Org Chem
Gsell C, Rebmann P, Opara K, Beuck C, Bayer P, Bier D, Vetter IR, Schrader T.   +7 more
europepmc   +1 more source

Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2‐COL3A1 axis

Molecular Oncology, EarlyView.
CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak, Iva Staniczková Zambo, Matěj Přikryl, Peter Múdry, Danica Zapletalová, Jarmila Navrátilová, Jiří Navrátil, Jan Šmarda, Liudmyla Drobot, Petr Beneš, Lucia Knopfová   +10 more
wiley   +1 more source

Bacteriocin biophysics: From protein-protein interaction models to navigators of the bacterial cell envelope. [PDF]

J Biol Chem
Kleanthous C.
europepmc   +1 more source

Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy

Molecular Oncology, EarlyView.
Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen, Kristiane Søreng, Chiara Veroni, Laura Trachsel‐Moncho, Nagham Asp, Robin Gaupset, Lars Gustav Lyckander, Helene Knævelsrud, Lars Eftang, Anne Simonsen   +9 more
wiley   +1 more source

Disrupting the KRAS-SOS1 protein-protein interaction: mechanistic rationale for pan-KRAS pathway suppression and combination therapy. [PDF]

Front Chem
Kamel EM, Khadrawy SM, Ali MAM, Abukhadra MR, Yassin NYS, Alkhedhairi S, Aba Alkhayl FF, Lamsabhi AM.   +7 more
europepmc   +1 more source