PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29970878-5 2018 The underlying mechanisms were revealed that knockdown of YY1 downregulated both S473 and T308 phosphorylation of AKT (protein kinase B), which was mainly responsible for cisplatin resistance, whereas overexpression of YY1 upregulated both S473 and T308 phosphorylation. Cisplatin 171-180 protein tyrosine kinase 2 beta Homo sapiens 119-135 30417422-11 2019 Furthermore, ADAMTS18 suppressed epidermal growth factor receptor/protein kinase B (EGFR/AKT) signaling, which sensitized lung cancer cells to cisplatin. Cisplatin 143-152 protein tyrosine kinase 2 beta Homo sapiens 66-82 27581532-7 2016 When phosphatidylinositol 3-kinase/protein kinase B signaling was inhibited by corresponding inhibitors, PD-L1 expression was downregulated and apoptosis was upregulated in the cisplatin-treated cancer cells. Cisplatin 177-186 protein tyrosine kinase 2 beta Homo sapiens 35-51 29518977-4 2018 By combining statistical methods with available gene annotations and without a previously defined hypothesis HRas, MAPK14 (p38), CCL2, DOK1 and PTK2B were identified as genes possibly relevant for cisplatin resistance. Cisplatin 197-206 protein tyrosine kinase 2 beta Homo sapiens 144-149 29518977-6 2018 HRas, p38, CCL2, DOK1, PTK2B and JNK3 were integrated into a model of resistance-associated signalling alterations describing differential gene and protein expression between cisplatin-sensitive and -resistant cells in reaction to cisplatin exposure. Cisplatin 175-184 protein tyrosine kinase 2 beta Homo sapiens 23-28 29518977-6 2018 HRas, p38, CCL2, DOK1, PTK2B and JNK3 were integrated into a model of resistance-associated signalling alterations describing differential gene and protein expression between cisplatin-sensitive and -resistant cells in reaction to cisplatin exposure. Cisplatin 231-240 protein tyrosine kinase 2 beta Homo sapiens 23-28 24960055-0 2014 Hexabromocyclododecane and polychlorinated biphenyls increase resistance of hepatocellular carcinoma cells to cisplatin through the phosphatidylinositol 3-kinase/protein kinase B pathway. Cisplatin 110-119 protein tyrosine kinase 2 beta Homo sapiens 162-178 34411338-6 2021 Results showed that MSeA substantially attenuated cisplatin-induced PD-L1 expression via inhibiting protein kinase B phosphorylation, thereby potentiated cisplatin cytotoxicity in prostate and lung cancer cell models. Cisplatin 50-59 protein tyrosine kinase 2 beta Homo sapiens 100-116 19880522-15 2010 Moreover, Pyk2 FERM expression in human fibroblasts upon FAK knockdown prevented cisplatin-mediated apoptosis. Cisplatin 81-90 protein tyrosine kinase 2 beta Homo sapiens 10-14 10187797-3 1999 Here we demonstrate that pp125 focal adhesion kinase-related tyrosine kinase RAFTK (also known as PYK2, CADTK) is activated specifically by methylmethane sulfonate (MMS) and hyperosmolarity but not by ultraviolet radiation, ionizing radiation, or cis-platinum. Cisplatin 247-259 protein tyrosine kinase 2 beta Homo sapiens 77-82 10187797-3 1999 Here we demonstrate that pp125 focal adhesion kinase-related tyrosine kinase RAFTK (also known as PYK2, CADTK) is activated specifically by methylmethane sulfonate (MMS) and hyperosmolarity but not by ultraviolet radiation, ionizing radiation, or cis-platinum. Cisplatin 247-259 protein tyrosine kinase 2 beta Homo sapiens 98-102 10187797-3 1999 Here we demonstrate that pp125 focal adhesion kinase-related tyrosine kinase RAFTK (also known as PYK2, CADTK) is activated specifically by methylmethane sulfonate (MMS) and hyperosmolarity but not by ultraviolet radiation, ionizing radiation, or cis-platinum. Cisplatin 247-259 protein tyrosine kinase 2 beta Homo sapiens 104-109 33813077-11 2021 Functional analysis indicated that CHD1L knockdown clearly restrained the activation of ERK1/2, protein kinase B (AKT) and NF-kappaB signaling pathways in cDDP-resistant OS cells. Cisplatin 155-159 protein tyrosine kinase 2 beta Homo sapiens 96-112 34774850-9 2022 The results for in vitro and vivo assays revealed that the knockdown of Flotillin-1 could significantly inhibit the proliferation of GC cells and increased the sensitivity of GC cells to cisplatin via the regulation of the protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) signaling pathway. Cisplatin 187-196 protein tyrosine kinase 2 beta Homo sapiens 223-239 34277781-11 2021 The experiment shows that ROPPIP can up-regulate the expression levels of MMP2, Ki67, and Bcl2 in HTR-8/Svneo cells, down-regulate the expression of caspase-3, promote the proliferation and migration of HTR-8/Svneo cells and inhibit the apoptosis induced by cisplatin, the activation of the phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway may be associated with the function of ROPPIP. Cisplatin 258-267 protein tyrosine kinase 2 beta Homo sapiens 321-337 34313839-13 2021 Pyk2 knockdown enhanced the sensitivity to cisplatin in ESCC cells. Cisplatin 43-52 protein tyrosine kinase 2 beta Homo sapiens 0-4 34522245-11 2021 After cisplatin treatment, down-regulation of BANCR could consequently attenuate TU686-DDP-R and TU177-DDP-R cell proliferation, and the expression of MRP1, Bcl-2, and p-PKB was decreased and Bax was increased. Cisplatin 6-15 protein tyrosine kinase 2 beta Homo sapiens 170-173 35256453-1 2022 Cisplatin-induced ototoxicity can be partially attributed to excessive reactive oxygen species (ROS) production, and agmatine is well-known for the activation of the phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT) pathway to inhibit ROS production. Cisplatin 0-9 protein tyrosine kinase 2 beta Homo sapiens 199-215 35628594-6 2022 In addition, nimodipine pre-treatment counteracted the reduction in LIM Domain Only 4 (LMO4) by cisplatin, which was associated with increased activation of Ak strain transforming/protein kinase B (Akt), cAMP response element-binding protein (CREB), and signal transducers and activators of transcription 3 (Stat3). Cisplatin 96-105 protein tyrosine kinase 2 beta Homo sapiens 180-196 31814556-8 2020 Conversely, Rh2 was found to repress cisplatin-induced phosphorylation of epidermal growth factor receptor, phosphoinositide 3-kinase, protein kinase B, and autophagy. Cisplatin 37-46 protein tyrosine kinase 2 beta Homo sapiens 135-151 35238281-2 2022 We found that ataxia-telangiectasia mutated (ATM), ataxia-telangiectasia and Rad3-related (ATR) and DNA-dependent protein kinase catalytic subunit (DNA-PKcs) of DNA repair kinases and signal transduction molecules, protein kinase B (AKT)/target mammalian target of rapamycin (mTOR), were significantly phosphorylated in cisplatin-resistant wtEGFR NSCLC cell lines (H358R and A549R) than in their parental cells. Cisplatin 320-329 protein tyrosine kinase 2 beta Homo sapiens 215-231 35196205-3 2022 The purpose of this study was to explore the effects of circRNA SET domain protein 3 (circSETD3) on protein kinase B (Akt)/ mammalian target of rapamycin (mTOR) signaling pathway and cisplatin (DDP) resistance to NPC and explore its downstream mechanism. Cisplatin 194-197 protein tyrosine kinase 2 beta Homo sapiens 100-116 32945500-1 2020 The high activation of protein kinase B (AKT)/nuclear factor-kappaB (NF-kappaB) signaling has often been associated with the induction of non-small cell lung cancer (NSCLC) cell survival and resistance to cisplatin, which is one of the most widely used chemotherapeutic drugs in the treatment of NSCLC. Cisplatin 205-214 protein tyrosine kinase 2 beta Homo sapiens 23-39 32627280-9 2020 Activation of protein kinase B (Akt) pathway attenuated the effect of deoxyshikonin on cisplatin resistance and ABCB1 expression and function in A549/cis and H1299/cis cells. Cisplatin 87-96 protein tyrosine kinase 2 beta Homo sapiens 14-30 33024577-4 2020 Here, we found that, in CCA cells, when cisplatin (CDDP) displayed anti-tumor effects, it activated 14-3-3epsilon simultaneously, which in turn formed a survival mechanism via the phosphorylation of phosphatidylinositol 3-kinase/protein kinase B (PI-3K/Akt). Cisplatin 40-49 protein tyrosine kinase 2 beta Homo sapiens 229-245 33024577-4 2020 Here, we found that, in CCA cells, when cisplatin (CDDP) displayed anti-tumor effects, it activated 14-3-3epsilon simultaneously, which in turn formed a survival mechanism via the phosphorylation of phosphatidylinositol 3-kinase/protein kinase B (PI-3K/Akt). Cisplatin 51-55 protein tyrosine kinase 2 beta Homo sapiens 229-245