Results 121 to 130 of about 4,965,955 (309)

TEC Expresses Highly in Hepatocellular Carcinoma and Is Involved in Drug Resistance

Zhongliu Fangzhi Yanjiu, 2018
Objective To investigate the expression level of TEC, a no-receptor tyrosine kinase, in hepatocellular carcinoma(HCC) tissues and its correlation with drug resistance.
LIU Wen, LI Feifei, ZHONG Minggui, LIU Yakun, FANG Haoshu, WANG Siying   +5 more
doaj   +1 more source

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

Molecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura, Tadahiro Kuribayashi, Johannes Brägelmann, Sachi Okawa, Masataka Taoka, Shunta Mori, Tomoka Nishimura, Takaaki Tanaka, Go Makimoto, Kiichiro Ninomiya, Kammei Rai, Eiki Ichihara, Ryohei Katayama, Katsuyuki Hotta, Masahiro Tabata, Yosuke Togashi, Yoshinobu Maeda, Martin L. Sos, Katsuyuki Kiura, Kadoaki Ohashi   +19 more
wiley   +1 more source

Protein Kinase Inhibitors

Folia Biologica, 2006
Since protein kinases have been found to be implicated in many diseases, first of all malignancies, they are considered as promising therapeutic targets. Many protein kinase inhibitors have been designed by now. These molecules have a low molecular weight and most of them bind to protein kinases competing with ATP for the ATP-binding site. Some protein
I, Shchemelinin, L, Sefc, E, Necas
openaire   +2 more sources

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

Role of p38 mitogen-activated protein kinase isoforms in murine skin inflammation induced by 12-O-tetradecanoylphorbol 13-acetate [PDF]

, 2011
p38 mitogen-activated protein kinase plays a pivotal role in skin inflammation. The purpose of this study was to investigate the role of the various p38 isoforms. p38 beta/delta-knockout-C57BL/6 mice were generated, studied in a 12-O-tetradecanoylphorbol
Iversen, Lars, A Funding, JS Arthur, Johansen, Claus, Kragballe, Knud, BM Bibby, Lilleholt, Louise Langer, Funding, Anne, L Iversen, Bibby, Bo Martin, K Kragballe, C Johansen, Arthur, J. Simon C.; id_orcid, LL Lilleholt   +13 more
core   +1 more source

Regulation of Nicotiana tabacum osmotic stress-activated protein kinase and its cellular partner GAPDH by nitric oxide in response to salinity [PDF]

, 2010
Several studies focused on elucidating the mechanism of nitric oxide (NO) signalling in plant cells highlighted that its biological effects are partly mediated by protein kinases. Identity of these kinases and details of how NO modulates their activities,
Dobrowolska, Grażyna
core   +1 more source

GSK-3 inhibitors: preclinical and clinical focus on CNS

Frontiers in Molecular Neuroscience, 2011
Inhibiting glycogen synthase kinase-3 (GSK-3) activity via pharmacological intervention has become an important target for treating neurodegenerative and psychiatric disorders.
Hagit eEldar-Finkelman, Ana eMartinez
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

MITF maintains genome stability in nonmelanocyte lineages

Molecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir, Adrián López García de Lomana, Thejus B. Venkatesh, Kritika Kirty, Snaevar Sigurdsson, Linda Vidarsdottir, Ramile Dilshat, Erla Sveinbjornsdottir, Snaedis Ragnarsdottir, Daniel H Magnusson, Maria R. Bustos, Eirikur Steingrimsson, Thorkell Gudjonsson, Stefan Sigurdsson   +13 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