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Journal articles on the topic 'Tyrosine Kinase (RTK) Pathway'

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Published: 4 June 2021

Last updated: 6 September 2023

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1

Fraser, Jane, Ainara G. Cabodevilla, Joanne Simpson, and Noor Gammoh. "Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking." Essays in Biochemistry 61, no. 6 (2017): 597–607. http://dx.doi.org/10.1042/ebc20170091.

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Vesicular trafficking events play key roles in the compartmentalization and proper sorting of cellular components. These events have crucial roles in sensing external signals, regulating protein activities and stimulating cell growth or death decisions. Although mutations in vesicle trafficking players are not direct drivers of cellular transformation, their activities are important in facilitating oncogenic pathways. One such pathway is the sensing of external stimuli and signalling through receptor tyrosine kinases (RTKs). The regulation of RTK activity by the endocytic pathway has been exte

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Li, X., L. Wheldon, and J. K. Heath. "Sprouty: a controversial role in receptor tyrosine kinase signalling pathways." Biochemical Society Transactions 31, no. 6 (2003): 1445–46. http://dx.doi.org/10.1042/bst0311445.

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Sprouty was first identified in Drosophila as a novel antagonist of the fibroblast growth factor signalling pathway. Sprouty proteins comprise a big family, members of which are characterized by a cysteine-rich domain which confers inhibitory activity, whereas differences in the N-terminal region may be responsible for functional divergence. The role of Sprouty in RTK (receptor tyrosine kinase) signalling pathways is still controversial. Sprouty may negatively or positively regulate RTK signalling via differential interaction with different signalling molecules, and hence exert different mecha

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Myers, Andrea Pomrehn, Laura B. Corson, Janet Rossant, and Julie C. Baker. "Characterization of Mouse Rsk4 as an Inhibitor of Fibroblast Growth Factor-RAS-Extracellular Signal-Regulated Kinase Signaling." Molecular and Cellular Biology 24, no. 10 (2004): 4255–66. http://dx.doi.org/10.1128/mcb.24.10.4255-4266.2004.

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ABSTRACT Receptor tyrosine kinase (RTK) signals regulate the specification of a varied array of tissue types by utilizing distinct modules of proteins to elicit diverse effects. The RSK proteins are part of the RTK signal transduction pathway and are thought to relay these signals by acting downstream of extracellular signal-regulated kinase (ERK). In this study we report the identification of ribosomal S6 kinase 4 (Rsk4) as an inhibitor of RTK signals. Among the RSK proteins, RTK inhibition is specific to RSK4 and, in accordance, is dependent upon a region of the RSK4 protein that is divergen

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He, Fang, Cong Chang, Bowen Liu, et al. "Copper (II) Ions Activate Ligand-Independent Receptor Tyrosine Kinase (RTK) Signaling Pathway." BioMed Research International 2019 (May 14, 2019): 1–8. http://dx.doi.org/10.1155/2019/4158415.

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Receptor tyrosine kinase (RTK) is activated by its natural ligand, mediating multiple essential biological processes. Copper (II) ions are bioactive ions and are crucial in the regulation of cell signaling pathway. However, the crosstalk between copper (II) ions and RTK-mediated cellular signaling remains unclear. Herein, we reported the effect of copper (II) ions on the ligand-independent RTK cellular signaling pathway. Our results indicate that both EGFR and MET signaling were activated by copper (II) in the absence of the corresponding ligands, EGF and HGF, respectively. Consequently, coppe

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Mamer, Spencer B., Alexandra A. Palasz, and P. I. Imoukhuede. "Mapping Tyrosine Kinase Receptor Dimerization to Receptor Expression and Ligand Affinities." Processes 7, no. 5 (2019): 288. http://dx.doi.org/10.3390/pr7050288.

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Tyrosine kinase receptor (RTK) ligation and dimerization is a key mechanism for translating external cell stimuli into internal signaling events. This process is critical to several key cell and physiological processes, such as in angiogenesis and embryogenesis, among others. While modulating RTK activation is a promising therapeutic target, RTK signaling axes have been shown to involve complicated interactions between ligands and receptors both within and across different protein families. In angiogenesis, for example, several signaling protein families, including vascular endothelial growth

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Fabian, JR, DK Morrison, and IO Daar. "Requirement for Raf and MAP kinase function during the meiotic maturation of Xenopus oocytes." Journal of Cell Biology 122, no. 3 (1993): 645–52. http://dx.doi.org/10.1083/jcb.122.3.645.

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The role of Raf and MAPK (mitogen-activated protein kinase) during the maturation of Xenopus oocytes was investigated. Treatment of oocytes with progesterone resulted in a shift in the electrophoretic mobility of Raf at the onset of germinal vesicle breakdown (GVBD), which was coincident with the activation of MAPK. Expression of a kinase-defective mutant of the human Raf-1 protein (KD-RAF) inhibited progesterone-mediated MAPK activation. MAPK activation was also inhibited by KD-Raf in oocytes expressing signal transducers of the receptor tyrosine kinase (RTK) pathway, including an activated t

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Taruno, Akiyuki, Naomi Niisato, and Yoshinori Marunaka. "Hypotonicity stimulates renal epithelial sodium transport by activating JNK via receptor tyrosine kinases." American Journal of Physiology-Renal Physiology 293, no. 1 (2007): F128—F138. http://dx.doi.org/10.1152/ajprenal.00011.2007.

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We previously reported that hypotonic stress stimulated transepithelial Na+ transport via a pathway dependent on protein tyrosine kinase (PTK; Niisato N, Van Driessche W, Liu M, Marunaka Y. J Membr Biol 175: 63–77, 2000). However, it is still unknown what type of PTK mediates this stimulation. In the present study, we investigated the role of receptor tyrosine kinase (RTK) in the hypotonic stimulation of Na+ transport. In renal epithelial A6 cells, we observed inhibitory effects of AG1478 [an inhibitor of the EGF receptor (EGFR)] and AG1296 [an inhibitor of the PDGF receptor (PDGFR)] on both t

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Smith, Rachel K., Pamela M. Carroll, John D. Allard, and Michael A. Simon. "MASK, a large ankyrin repeat and KH domain-containing protein involved inDrosophilareceptor tyrosine kinase signaling." Development 129, no. 1 (2002): 71–82. http://dx.doi.org/10.1242/dev.129.1.71.

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The receptor tyrosine kinases Sevenless (SEV) and the Epidermal growth factor receptor (EGFR) are required for the proper development of the Drosophila eye. The protein tyrosine phosphatase Corkscrew (CSW) is a common component of many RTK signaling pathways, and is required for signaling downstream of SEV and EGFR. In order to identify additional components of these signaling pathways, mutations that enhanced the phenotype of a dominant negative form of Corkscrew were isolated. This genetic screen identified the novel signaling molecule MASK, a large protein that contains two blocks of ankyri

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Liu, Zhi, Peng Hou, Meiju Ji, et al. "Highly Prevalent Genetic Alterations in Receptor Tyrosine Kinases and Phosphatidylinositol 3-Kinase/Akt and Mitogen-Activated Protein Kinase Pathways in Anaplastic and Follicular Thyroid Cancers." Journal of Clinical Endocrinology & Metabolism 93, no. 8 (2008): 3106–16. http://dx.doi.org/10.1210/jc.2008-0273.

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Abstract Context: Genetic alterations in receptor tyrosine kinases (RTKs) and phosphatidylinositol 3-kinase (PI3K)/Akt and MAPK pathways have not been fully defined in anaplastic and follicular thyroid cancers [anaplastic thyroid cancer (ATC), follicular thyroid cancer (FTC)]. Objective: The objective of the study was to explore a wide-range genetic basis for the involvement of these pathways in ATC. Design: We examined mutations and copy number gains of a large panel of genes in these pathways and corresponding phosphorylation of ERK (p-ERK) and Akt. Results: We found frequent copy gains of R

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Gonzalez-Magaldi, Monica, Jacqueline M. McCabe, Haley N. Cartwright, Ningze Sun, and Daniel J. Leahy. "Conserved roles for receptor tyrosine kinase extracellular regions in regulating receptor and pathway activity." Biochemical Journal 477, no. 21 (2020): 4207–20. http://dx.doi.org/10.1042/bcj20200702.

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Receptor Tyrosine Kinases (RTKs) comprise a diverse group of cell-surface receptors that mediate key signaling events during animal development and are frequently activated in cancer. We show here that deletion of the extracellular regions of 10 RTKs representing 7 RTK classes or their substitution with the dimeric immunoglobulin Fc region results in constitutive receptor phosphorylation but fails to result in phosphorylation of downstream signaling effectors Erk or Akt. Conversely, substitution of RTK extracellular regions with the extracellular region of the Epidermal Growth Factor Receptor

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Polzer, Harald, Hanna Janke, Wolfgang Hiddemann, Dirk Eick, and Karsten Spiekermann. "CBL Deletion Mutant Found in AML Patients Cause Transformation of Receptor Tyrosine Kinase Class III Expressing Cells by Activation of the AKT Pathway." Blood 118, no. 21 (2011): 2447. http://dx.doi.org/10.1182/blood.v118.21.2447.2447.

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Abstract Abstract 2447 We examined the oncogenic potential of CBL deletion mutant found in AML patients in cytokine receptor and receptor tyrosine kinase (RTKs) expressing cells. In addition, we analyzed the interaction sites of FLT3/CBL and the critical pathways activated by CBL deletion mutants. RTK, CBL and AKT constructs were expressed in Ba/F3 cells via a retroviral expression vector. Stable protein expression after transduction and fluorescence-activated cell sorting (FACS) was confirmed by western blotting and cellsurface-marker expression of receptors by flow cytometry. Cell Proliferat

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Li, Willis X., Herve Agaisse, Bernard Mathey-Prevot, and Norbert Perrimon. "Differential requirement for STAT by gain-of-function and wild-type receptor tyrosine kinase Torso in Drosophila." Development 129, no. 18 (2002): 4241–48. http://dx.doi.org/10.1242/dev.129.18.4241.

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Malignant transformation frequently involves aberrant signaling from receptor tyrosine kinases (RTKs). These receptors commonly activate Ras/Raf/MEK/MAPK signaling but when overactivated can also induce the JAK/STAT pathway, originally identified as the signaling cascade downstream of cytokine receptors. Inappropriate activation of STAT has been found in many human cancers. However, the contribution of the JAK/STAT pathway in RTK signaling remains unclear. We have investigated the requirement of the JAK/STAT pathway for signaling by wild-type and mutant forms of the RTK Torso (Tor) using a gen

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Ariss, Majd M., Alexander R. Terry, Abul B. M. M. K. Islam, Nissim Hay, and Maxim V. Frolov. "Amalgam regulates the receptor tyrosine kinase pathway through Sprouty in glial cell development in the Drosophila larval brain." Journal of Cell Science 133, no. 19 (2020): jcs250837. http://dx.doi.org/10.1242/jcs.250837.

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ABSTRACTThe receptor tyrosine kinase (RTK) pathway plays an essential role in development and disease by controlling cell proliferation and differentiation. Here, we profile the Drosophila larval brain by single-cell RNA-sequencing and identify Amalgam (Ama), which encodes a cell adhesion protein of the immunoglobulin IgLON family, as regulating the RTK pathway activity during glial cell development. Depletion of Ama reduces cell proliferation, affects glial cell type composition and disrupts the blood–brain barrier (BBB), which leads to hemocyte infiltration and neuronal death. We show that A

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Yang, Wenli, Junlan Zhang, Bingqian Hu, et al. "The role of receptor tyrosine kinase activation in cholangiocytes and pulmonary vascular endothelium in experimental hepatopulmonary syndrome." American Journal of Physiology-Gastrointestinal and Liver Physiology 306, no. 1 (2014): G72—G80. http://dx.doi.org/10.1152/ajpgi.00178.2013.

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Pulmonary vascular dilation and angiogenesis underlie experimental hepatopulmonary syndrome (HPS) induced by common bile duct ligation (CBDL) and may respond to receptor tyrosine kinase (RTK) inhibition. Vascular endothelial growth factor-A (VEGF-A) expression occurs in proliferating cholangiocytes and pulmonary intravascular monocytes after CBDL, the latter contributing to angiogenesis. CBDL cholangiocytes also produce endothelin-1 (ET-1), which triggers lung vascular endothelin B receptor-mediated endothelial nitric oxide synthase (eNOS) activation and pulmonary intravascular monocyte accumu

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Azad, Taha, Reza Rezaei, Abera Surendran, et al. "Hippo Signaling Pathway as a Central Mediator of Receptors Tyrosine Kinases (RTKs) in Tumorigenesis." Cancers 12, no. 8 (2020): 2042. http://dx.doi.org/10.3390/cancers12082042.

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The Hippo pathway plays a critical role in tissue and organ growth under normal physiological conditions, and its dysregulation in malignant growth has made it an attractive target for therapeutic intervention in the fight against cancer. To date, its complex signaling mechanisms have made it difficult to identify strong therapeutic candidates. Hippo signaling is largely carried out by two main activated signaling pathways involving receptor tyrosine kinases (RTKs)—the RTK/RAS/PI3K and the RTK-RAS-MAPK pathways. However, several RTKs have also been shown to regulate this pathway to engage down

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Zhang, Si Qing, William G. Tsiaras, Toshiyuki Araki, et al. "Receptor-Specific Regulation of Phosphatidylinositol 3′-Kinase Activation by the Protein Tyrosine Phosphatase Shp2." Molecular and Cellular Biology 22, no. 12 (2002): 4062–72. http://dx.doi.org/10.1128/mcb.22.12.4062-4072.2002.

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ABSTRACT Receptor tyrosine kinases (RTKs) play distinct roles in multiple biological systems. Many RTKs transmit similar signals, raising questions about how specificity is achieved. One potential mechanism for RTK specificity is control of the magnitude and kinetics of activation of downstream pathways. We have found that the protein tyrosine phosphatase Shp2 regulates the strength and duration of phosphatidylinositol 3′-kinase (PI3K) activation in the epidermal growth factor (EGF) receptor signaling pathway. Shp2 mutant fibroblasts exhibit increased association of the p85 subunit of PI3K wit

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Nanri, Tomoko, Naofumi Matsuno, Toshiro Kawakita, et al. "Mutations in the Receptor Tyrosine Kinase Pathway Are Associated with Clinical Outcome in Patients with Acute Myeloblastic Leukemia Harboring t(8;21)(q22;q22)." Blood 104, no. 11 (2004): 3000. http://dx.doi.org/10.1182/blood.v104.11.3000.3000.

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Abstract AML1-MTG8 generated by t(8;21)(q22;q22) contributes to leukemic transformation but additional events are required for full leukemogenesis. We examined whether mutations in the receptor tyrosine kinase (RTK) pathway could be the genetic events that cause acute myeloblastic leukemia (AML) harboring t(8;21). Mutations in the second tyrosine kinase domain, juxtamembrane domain and exon 8 of the C-KIT gene were observed in 7, 1 and 3 of 37 AML patients with t(8;21), respectively. Three patients showed an internal tandem duplication in the juxtamembrane domain of the FLT3 gene. One patient

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Yang, Jun, Xin Liu, Susan Nyland, et al. "Platelet-Derived Growth Factor (PDGF)-BB Mediates Survival of Leukemic Large Granular Lymphocyte Via An Autocrine Regulatory Pathway." Blood 112, no. 11 (2008): 3803. http://dx.doi.org/10.1182/blood.v112.11.3803.3803.

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Abstract Tumor cells may stimulate their own proliferation through an autocrine mechanism by simultaneously producing growth factors and growth factor receptors. Proto-oncogene Platelet derived growth factor (PDGF) is a multifunctional molecule with roles in cell growth, proliferation, chemotaxis, actin reorganization and apoptosis resistance. PDGF exerts its cellular effects by inducing homo- or hetero-dimeric complex of α- or β-tyrosine kinase receptors, mediating its receptor tyrosine kinase (PDGF-β RTK) auto-phosphorylation, and consequently initiating downstream survival signaling pathway

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Hamilton, T. Guy, Richard A. Klinghoffer, Philip D. Corrin, and Philippe Soriano. "Evolutionary Divergence of Platelet-Derived Growth Factor Alpha Receptor Signaling Mechanisms." Molecular and Cellular Biology 23, no. 11 (2003): 4013–25. http://dx.doi.org/10.1128/mcb.23.11.4013-4025.2003.

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ABSTRACT Receptor tyrosine kinases (RTKs) direct diverse cellular and developmental responses by stimulating a relatively small number of overlapping signaling pathways. Specificity may be determined by RTK expression patterns or by differential activation of individual signaling pathways. To address this issue we generated knock-in mice in which the extracellular domain of the mouse platelet-derived growth factor alpha receptor (PDGFαR) is fused to the cytosolic domain of Drosophila Torso (αTor) or the mouse fibroblast growth factor receptor 1 (αFR). αTor homozygous embryos exhibit significan

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Shi, Tiezhu, Linli Yao, Ying Han, Piliang Hao, and Pengfei Lu. "Quantitative Phosphoproteomics Reveals System-Wide Phosphorylation Network Altered by Spry in Mouse Mammary Stromal Fibroblasts." International Journal of Molecular Sciences 20, no. 21 (2019): 5400. http://dx.doi.org/10.3390/ijms20215400.

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Understanding the fundamental role of the stroma in normal development and cancer progression has been an emerging focus in recent years. The receptor tyrosine kinase (RTK) signaling pathway has been reported playing critical roles in regulating the normal and cancer microenvironment, but the underlying mechanism is still not very clear. By applying the quantitative phosphoproteomic analysis of Sprouty proteins (SPRYs), generic modulators of RTK signaling and deleted mouse mammary fibroblasts, we quantified a total of 11,215 unique phosphorylation sites. By contrast, 554 phosphorylation sites

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Wu, Xinyan, Li Wang, Nicole A. Pearson, et al. "Quantitative Tyrosine Phosphoproteome Profiling of AXL Receptor Tyrosine Kinase Signaling Network." Cancers 13, no. 16 (2021): 4234. http://dx.doi.org/10.3390/cancers13164234.

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Overexpression and amplification of AXL receptor tyrosine kinase (RTK) has been found in several hematologic and solid malignancies. Activation of AXL can enhance tumor-promoting processes such as cancer cell proliferation, migration, invasion and survival. Despite the important role of AXL in cancer development, a deep and quantitative mapping of its temporal dynamic signaling transduction has not yet been reported. Here, we used a TMT labeling-based quantitative proteomics approach to characterize the temporal dynamics of the phosphotyrosine proteome induced by AXL activation. We identified

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Tanaka, Mai, and Dietmar W. Siemann. "Therapeutic Targeting of the Gas6/Axl Signaling Pathway in Cancer." International Journal of Molecular Sciences 22, no. 18 (2021): 9953. http://dx.doi.org/10.3390/ijms22189953.

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Many signaling pathways are dysregulated in cancer cells and the host tumor microenvironment. Aberrant receptor tyrosine kinase (RTK) pathways promote cancer development, progression, and metastasis. Hence, numerous therapeutic interventions targeting RTKs have been actively pursued. Axl is an RTK that belongs to the Tyro3, Axl, MerTK (TAM) subfamily. Axl binds to a high affinity ligand growth arrest specific 6 (Gas6) that belongs to the vitamin K-dependent family of proteins. The Gas6/Axl signaling pathway has been implicated to promote progression, metastasis, immune evasion, and therapeutic

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Lu, Bo, Eric T. Shinohara, Eric Edwards, Ling Geng, Jiahuai Tan, and Dennis E. Hallahan. "The Use of Tyrosine Kinase Inhibitors in Modifying the Response of Tumor Microvasculature to Radiotherapy." Technology in Cancer Research & Treatment 4, no. 6 (2005): 691–98. http://dx.doi.org/10.1177/153303460500400614.

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The response of the tumor microvasculature to ionizing radiation can be modified to improve tumor control in preclinical mouse models of cancer. Recent studies have shown that a variety of cancer drugs can improve the response of cancers to radiotherapy. Protein tyrosine kinase inhibitors (TKIs) have been shown to enhance radiation-induced destruction of tumor blood vessels. Among these compounds are inhibitors of a broad spectrum of receptor tyrosine kinases (RTKs). Inhibition of RTKs attenuates downstream signaling from various angiogenic growth factors, including vascular endothelial growth

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Reich, A., A. Sapir, and B. Shilo. "Sprouty is a general inhibitor of receptor tyrosine kinase signaling." Development 126, no. 18 (1999): 4139–47. http://dx.doi.org/10.1242/dev.126.18.4139.

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Sprouty was originally identified as an inhibitor of Drosophila FGF receptor signaling during tracheal development. By following the capacity of ectopic Sprouty to abolish the pattern of activated MAP kinase in embryos, we show that Sprouty can inhibit other receptor tyrosine kinase (RTK) signaling pathways, namely the Heartless FGF receptor and the EGF receptor. Similarly, in wing imaginal discs, ectopic Sprouty abolishes activated MAP kinase induced by the EGF receptor pathway. Sprouty expression is induced by the EGFR pathway in some, but not all, tissues in which EGFR is activated, most no

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Bunda, Severa, Pardeep Heir, Annie Li, Mamatjan Yasin, Gelareh Zadeh, and Kenneth Aldape. "CSIG-07. c-Src PHOSPHORYLATES AND INACTIVATES THE CIC TUMOR SUPPRESSOR PROTEIN IN GLIOBLASTOMA." Neuro-Oncology 22, Supplement_2 (2020): ii29. http://dx.doi.org/10.1093/neuonc/noaa215.119.

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Abstract Capicua (CIC) is a transcriptional repressor that counteracts activation of genes in response to receptor tyrosine kinase (RTK)/Ras/MEK/ERK signaling. Following activation of RTK, ERK enters the nucleus and serine-phosphorylates CIC, releasing it from its targets to permit gene expression. We recently showed that ERK triggers ubiquitin-mediated degradation of CIC in glioblastoma (GBM). In this study, we examined whether another important downstream effector of RTK/EGFR, the non-receptor tyrosine kinase c-Src, affects CIC repressor function in GBM. We found that c-Src binds and tyrosin

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Toffalini, Federica, and Jean-Baptiste Demoulin. "New insights into the mechanisms of hematopoietic cell transformation by activated receptor tyrosine kinases." Blood 116, no. 14 (2010): 2429–37. http://dx.doi.org/10.1182/blood-2010-04-279752.

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Abstract A large number of alterations in genes encoding receptor tyrosine kinase (RTK), namely FLT3, c-KIT, platelet-derived growth factor (PDGF) receptors, fibroblast growth factor (FGF) receptors, and the anaplastic large cell lymphoma kinase (ALK), have been found in hematopoietic malignancies. They have drawn much attention after the development of tyrosine kinase inhibitors. RTK gene alterations include point mutations and gene fusions that result from chromosomal rearrangements. In both cases, they activate the kinase domain in the absence of ligand, producing a permanent signal for cel

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Ledda, Fernanda, and Gustavo Paratcha. "Negative Regulation of Receptor Tyrosine Kinase (RTK) Signaling: A Developing Field." Biomarker Insights 2 (January 2007): 117727190700200. http://dx.doi.org/10.1177/117727190700200029.

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Trophic factors control cellular physiology by activating specific receptor tyrosine kinases (RTKs). While the over activation of RTK signaling pathways is associated with cell growth and cancer, recent findings support the concept that impaired down-regulation or deactivation of RTKs may also be a mechanism involved in tumor formation. Under this perspective, the molecular determinants of RTK signaling inhibition may act as tumor-suppressor genes and have a potential role as tumor markers to monitor and predict disease progression. Here, we review the current understanding of the physiologica

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Hamlet, Michelle R. Johnson, and Lizabeth A. Perkins. "Analysis of Corkscrew Signaling in the Drosophila Epidermal Growth Factor Receptor Pathway During Myogenesis." Genetics 159, no. 3 (2001): 1073–87. http://dx.doi.org/10.1093/genetics/159.3.1073.

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AbstractThe Drosophila nonreceptor protein tyrosine phosphatase, Corkscrew (Csw), functions positively in multiple receptor tyrosine kinase (RTK) pathways, including signaling by the epidermal growth factor receptor (EGFR). Detailed phenotypic analyses of csw mutations have revealed that Csw activity is required in many of the same developmental processes that require EGFR function. However, it is still unclear where in the signaling hierarchy Csw functions relative to other proteins whose activities are also required downstream of the receptor. To address this issue, genetic interaction exper

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Kimura, Mitsutoshi, Kazuki Kurihara, Hajime Moteki, and Masahiko Ogihara. "Growth Hormone Signaling Pathway Leading to the Induction of DNA Synthesis and Proliferation in Primary Cultured Hepatocytes of Adult Rats." Journal of Pharmacy & Pharmaceutical Sciences 24 (January 11, 2021): 1–15. http://dx.doi.org/10.18433/jpps31586.

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Background: We investigated the signal transduction pathway associated with growth hormone (GH)-stimulated DNA synthesis and proliferation in primary cultured hepatocytes. Methods: Adult rat hepatocytes were isolated from normal livers by two-step in situ collagenase perfusion to facilitate disaggregation of the adult rat liver. Then hepatocytes were cultured in serum-free Williams’ medium E supplemented with GH (1-100 ng/ml) in the presence or absence of test reagents. GH-induced hepatocyte DNA synthesis and proliferation were determined, and the phosphorylation activities of Janus kinase (JA

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Starchenko, Alina, Ramona Graves-Deal, Douglas Brubaker та ін. "Cell surface integrin α5ß1 clustering negatively regulates receptor tyrosine kinase signaling in colorectal cancer cells via glycogen synthase kinase 3". Integrative Biology 13, № 6 (2021): 153–66. http://dx.doi.org/10.1093/intbio/zyab009.

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Abstract As a key process within the tissue microenvironment, integrin signaling can influence cell functional responses to growth factor stimuli. We show here that clustering of integrin α5ß1 at the plasma membrane of colorectal cancer-derived epithelial cells modulates their ability to respond to stimulation by receptor tyrosine kinase (RTK)-activating growth factors EGF, NRG and HGF, through GSK3-mediated suppression of Akt pathway. We observed that integrin α5ß1 is lost from the membrane of poorly organized human colorectal tumors and that treatment with the integrin-clustering antibody P4

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Mineo, Alessandro, Marc Furriols, and Jordi Casanova. "The trigger (and the restriction) of Torso RTK activation." Open Biology 8, no. 12 (2018): 180180. http://dx.doi.org/10.1098/rsob.180180.

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The Torso pathway is an ideal model of receptor tyrosine kinase systems, in particular when addressing questions such as how receptor activity is turned on and, equally important, how it is restricted, how different outcomes can be generated from a single signal, and the extent to which gene regulation by signalling pathways relies on the relief of transcriptional repression. In this regard, we considered it pertinent to single out the fundamental notions learned from the Torso pathway beyond the specificities of this system (Furriols and Casanova 2003 EMBO J. 22 , 1947–1952. ( doi:10.1093/emb

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Lim, Young-Mi, Leo Tsuda, Yoshihiro H. Inoue, et al. "Dominant Mutations of Drosophila MAP Kinase Kinase and Their Activities in Drosophila and Yeast MAP Kinase Cascades." Genetics 146, no. 1 (1997): 263–73. http://dx.doi.org/10.1093/genetics/146.1.263.

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Eight alleles of Dsor1 encoding a Drosophila homologue of mitogen-activated protein (MAP) kinase kinase were obtained as dominant suppressors of the MAP kinase kinase kinase D-raf. These Dsor1 alleles themselves showed no obvious phenotypic consequences nor any effect on the viability of the flies, although they were highly sensitive to upstream signals and strongly interacted with gain-of-function mutations of upstream factors. They suppressed mutations for receptor tyrosine kinases (RTKs); torso (tor), sevenless (sev) and to a lesser extent Drosophila EGF receptor (DER). Furthermore, the Dso

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Duan, Yi, Johannes Haybaeck, and Zhihui Yang. "Therapeutic Potential of PI3K/AKT/mTOR Pathway in Gastrointestinal Stromal Tumors: Rationale and Progress." Cancers 12, no. 10 (2020): 2972. http://dx.doi.org/10.3390/cancers12102972.

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Gastrointestinal stromal tumor (GIST) originates from interstitial cells of Cajal (ICCs) in the myenteric plexus of the gastrointestinal tract. Most GISTs arise due to mutations of KIT and PDGFRA gene activation, encoding the receptor tyrosine kinase (RTK). The clinical use of the RTK inhibitor imatinib has significantly improved the management of GIST patients; however, imatinib resistance remains a challenge. The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway is a critical survival pathway for cell proliferation, apoptosis, autophagy

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Crose, Lisa E. S., and Corinne M. Linardic. "Receptor Tyrosine Kinases as Therapeutic Targets in Rhabdomyosarcoma." Sarcoma 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/756982.

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Rhabdomyosarcomas (RMSs) are the most common soft tissue sarcomas of childhood and adolescence. To date, there are no effective treatments that target the genetic abnormalities in RMS, and current treatment options for high-risk groups are not adequate. Over the past two decades, research into the molecular mechanisms of RMS has identified key genes and signaling pathways involved in disease pathogenesis. In these studies, members of the receptor tyrosine kinase (RTK) family of cell surface receptors have been characterized as druggable targets for RMS. Through small molecule inhibitors, ligan

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Rebay, Ilaria, Fangli Chen, Francis Hsiao, et al. "A Genetic Screen for Novel Components of the Ras/Mitogen-Activated Protein Kinase Signaling Pathway That Interact With the yan Gene of Drosophila Identifies split ends, a New RNA Recognition Motif-Containing Protein." Genetics 154, no. 2 (2000): 695–712. http://dx.doi.org/10.1093/genetics/154.2.695.

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Abstract The receptor tyrosine kinase (RTK) signaling pathway is used reiteratively during the development of all multicellular organisms. While the core RTK/Ras/MAPK signaling cassette has been studied extensively, little is known about the nature of the downstream targets of the pathway or how these effectors regulate the specificity of cellular responses. Drosophila yan is one of a few downstream components identified to date, functioning as an antagonist of the RTK/Ras/MAPK pathway. Previously, we have shown that ectopic expression of a constitutively active protein (yanACT) inhibits the d

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Wang, Y., J. P. Windham, R. A. Samul, et al. "Subgroup classification of receptor tyrosine kinase (RTK) pathway activation in KRAS-mutated metastatic carcinoma." Journal of Clinical Oncology 29, no. 15_suppl (2011): e18019-e18019. http://dx.doi.org/10.1200/jco.2011.29.15_suppl.e18019.

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Becker, Elena, Uyen Huynh-Do, Sacha Holland, Tony Pawson, Tom O. Daniel, and Edward Y. Skolnik. "Nck-Interacting Ste20 Kinase Couples Eph Receptors to c-Jun N-Terminal Kinase and Integrin Activation." Molecular and Cellular Biology 20, no. 5 (2000): 1537–45. http://dx.doi.org/10.1128/mcb.20.5.1537-1545.2000.

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ABSTRACT The mammalian Ste20 kinase Nck-interacting kinase (NIK) specifically activates the c-Jun amino-terminal kinase (JNK) mitogen-activated protein kinase module. NIK also binds the SH3 domains of the SH2/SH3 adapter protein Nck. To determine whether Nck functions as an adapter to couple NIK to a receptor tyrosine kinase signaling pathway, we determined whether NIK is activated by Eph receptors (EphR). EphRs constitute the largest family of receptor tyrosine kinases (RTK), and members of this family play important roles in patterning of the nervous and vascular systems. In this report, we

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Zhang, Qian, Qingxia Zheng, and Xiangyi Lu. "A Genetic Screen for Modifiers of Drosophila Src42A Identifies Mutations in Egfr, rolled and a Novel Signaling Gene." Genetics 151, no. 2 (1999): 697–711. http://dx.doi.org/10.1093/genetics/151.2.697.

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Abstract Drosophila Src42A, a close relative of the vertebrate c-Src, has been implicated in the Ras-Mapk signaling cascade. An allele of Src42A, Su(Raf)1, dominantly suppresses the lethality of partial loss-of-function Raf mutations. To isolate genes involved in the same pathway where Src42A functions, we carried out genetic screens for dominant suppressor mutations that prevented Su(Raf)1 from suppressing Raf. Thirty-six mutations representing at least five genetic loci were recovered from the second chromosome. These are Drosophila EGF Receptor (Egfr), rolled, Src42A, and two other new loci

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Balmaña, Meritxell, Francisca Diniz, Tália Feijão, Cristina C. Barrias, Stefan Mereiter та Celso A. Reis. "Analysis of the Effect of Increased α2,3-Sialylation on RTK Activation in MKN45 Gastric Cancer Spheroids Treated with Crizotinib". International Journal of Molecular Sciences 21, № 3 (2020): 722. http://dx.doi.org/10.3390/ijms21030722.

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In the scenario of personalized medicine, targeted therapies are currently the focus of cancer drug development. These drugs can block the growth and spread of tumor cells by interfering with key molecules involved in malignancy, such as receptor tyrosine kinases (RTKs). MET and Recepteur d’Origine Nantais (RON), which are RTKs frequently overactivated in gastric cancer, are glycoprotein receptors whose activation have been shown to be modulated by the cellular glycosylation. In this work, we address the role of sialylation in gastric cancer therapy using an innovative 3D high-throughput cell

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Michniewicz, Filip, Federica Saletta, Jourdin Rouen, David Ziegler, and Orazio Vittorio. "DIPG-83. USING COPPER CHELATING AGENTS TO TARGET RECEPTOR TYROSINE KINASE SIGNALLING IN DIFFUSE INTRINSIC PONTINE GLIOMA (DIPG)." Neuro-Oncology 22, Supplement_3 (2020): iii303. http://dx.doi.org/10.1093/neuonc/noaa222.124.

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Abstract DIPG is a universally fatal pediatric brain cancer. Receptor tyrosine kinase (RTK) pathway alterations are among the defining characteristics in many patients. Copper is a transition metal essential for cellular signaling, known to impact PI3K/AKT and MAPK/ERK pathways. Copper chelating agents are clinically approved for use in children with Wilson’s Disease, documented to reduce brain copper levels and are cited as potential cancer therapeutics. Due to copper’s wide cellular integration, we propose that targeting copper in DIPG through use of copper chelators is a viable therapeutic

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Almarán, Beatriz, Guillem Ramis, Silvia Fernández de Mattos, and Priam Villalonga. "Rnd3 Is a Crucial Mediator of the Invasive Phenotype of Glioblastoma Cells Downstream of Receptor Tyrosine Kinase Signalling." Cells 11, no. 23 (2022): 3716. http://dx.doi.org/10.3390/cells11233716.

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Enhanced invasiveness is one of the defining biological traits of glioblastoma cells, which exhibit an infiltrative nature that severely hinders surgical resection. Among the molecular lesions responsible for GBM aggressiveness, aberrant receptor tyrosine kinase (RTK) signalling is well-characterised. Enhanced RTK signalling directly impacts a myriad of cellular pathways and downstream effectors, which include the Rho GTPase family, key regulators of actin cytoskeletal dynamics. Here, we have analysed the functional crosstalk between oncogenic signals emanating from RTKs and Rho GTPases and fo

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Mele, Sarah, and Travis K. Johnson. "Receptor Tyrosine Kinases in Development: Insights from Drosophila." International Journal of Molecular Sciences 21, no. 1 (2019): 188. http://dx.doi.org/10.3390/ijms21010188.

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Cell-to-cell communication mediates a plethora of cellular decisions and behaviors that are crucial for the correct and robust development of multicellular organisms. Many of these signals are encoded in secreted hormones or growth factors that bind to and activate cell surface receptors, to transmit the cue intracellularly. One of the major superfamilies of cell surface receptors are the receptor tyrosine kinases (RTKs). For nearly half a century RTKs have been the focus of intensive study due to their ability to alter fundamental aspects of cell biology, such as cell proliferation, growth, a

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Tilak, Manali, Jennifer Holborn, Laura A. New, Jasmin Lalonde, and Nina Jones. "Receptor Tyrosine Kinase Signaling and Targeting in Glioblastoma Multiforme." International Journal of Molecular Sciences 22, no. 4 (2021): 1831. http://dx.doi.org/10.3390/ijms22041831.

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Glioblastoma multiforme (GBM) is amongst the deadliest of human cancers, with a median survival rate of just over one year following diagnosis. Characterized by rapid proliferation and diffuse infiltration into the brain, GBM is notoriously difficult to treat, with tumor cells showing limited response to existing therapies and eventually developing resistance to these interventions. As such, there is intense interest in better understanding the molecular alterations in GBM to guide the development of more efficient targeted therapies. GBM tumors can be classified into several molecular subtype

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Modzelewska, Katarzyna, Marc G. Elgort, Jingyu Huang, et al. "An Activating Mutation in sos-1 Identifies Its Dbl Domain as a Critical Inhibitor of the Epidermal Growth Factor Receptor Pathway during Caenorhabditis elegans Vulval Development." Molecular and Cellular Biology 27, no. 10 (2007): 3695–707. http://dx.doi.org/10.1128/mcb.01630-06.

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ABSTRACT Proper regulation of receptor tyrosine kinase (RTK)-Ras-mitogen-activated protein kinase (MAPK) signaling pathways is critical for normal development and the prevention of cancer. SOS is a dual-function guanine nucleotide exchange factor (GEF) that catalyzes exchange on Ras and Rac. Although the physiologic role of SOS and its CDC25 domain in RTK-mediated Ras activation is well established, the in vivo function of its Dbl Rac GEF domain is less clear. We have identified a novel gain-of-function missense mutation in the Dbl domain of Caenorhabditis elegans SOS-1 that promotes epidermal

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Guan, Jikui, Marcus Borenäs, Junfeng Xiong, Wei-Yun Lai, Ruth H. Palmer, and Bengt Hallberg. "IGF1R Contributes to Cell Proliferation in ALK-Mutated Neuroblastoma with Preference for Activating the PI3K-AKT Signaling Pathway." Cancers 15, no. 17 (2023): 4252. http://dx.doi.org/10.3390/cancers15174252.

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Aberrant activation of anaplastic lymphoma kinase (ALK) by activating point mutation or amplification drives 5–12% of neuroblastoma (NB). Previous work has identified the involvement of the insulin-like growth factor 1 receptor (IGF1R) receptor tyrosine kinase (RTK) in a wide range of cancers. We show here that many NB cell lines exhibit IGF1R activity, and that IGF1R inhibition led to decreased cell proliferation to varying degrees in ALK-driven NB cells. Furthermore, combined inhibition of ALK and IGF1R resulted in synergistic anti-proliferation effects, in particular in ALK-mutated NB cells

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Li, W., E. M. Skoulakis, R. L. Davis, and N. Perrimon. "The Drosophila 14–3-3 protein Leonardo enhances Torso signaling through D-Raf in a Ras 1-dependent manner." Development 124, no. 20 (1997): 4163–71. http://dx.doi.org/10.1242/dev.124.20.4163.

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14-3-3 proteins have been shown to interact with Raf-1 and cause its activation when overexpressed. However, their precise role in Raf-1 activation is still enigmatic, as they are ubiquitously present in cells and found to associate with Raf-1 in vivo regardless of its activation state. We have analyzed the function of the Drosophila 14–3-3 gene leonardo (leo) in the Torso (Tor) receptor tyrosine kinase (RTK) pathway. In the syncytial blastoderm embryo, activation of Tor triggers the Ras/Raf/MEK pathway that controls the transcription of tailless (tll). We find that, in the absence of Tor, ove

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Zinkle, Allen, and Moosa Mohammadi. "A threshold model for receptor tyrosine kinase signaling specificity and cell fate determination." F1000Research 7 (June 21, 2018): 872. http://dx.doi.org/10.12688/f1000research.14143.1.

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Upon ligand engagement, the single-pass transmembrane receptor tyrosine kinases (RTKs) dimerize to transmit qualitatively and quantitatively different intracellular signals that alter the transcriptional landscape and thereby determine the cellular response. The molecular mechanisms underlying these fundamental events are not well understood. Considering recent insights into the structural biology of fibroblast growth factor signaling, we propose a threshold model for RTK signaling specificity in which quantitative differences in the strength/longevity of ligand-induced receptor dimers on the

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Choe, Sung, Hongfang Wang, Courtney D. DiNardo, et al. "Molecular mechanisms mediating relapse following ivosidenib monotherapy in IDH1-mutant relapsed or refractory AML." Blood Advances 4, no. 9 (2020): 1894–905. http://dx.doi.org/10.1182/bloodadvances.2020001503.

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Abstract Isocitrate dehydrogenase (IDH) 1 and 2 mutations result in overproduction of D-2-hydroxyglutarate (2-HG) and impaired cellular differentiation. Ivosidenib, a targeted mutant IDH1 (mIDH1) enzyme inhibitor, can restore normal differentiation and results in clinical responses in a subset of patients with mIDH1 relapsed/refractory (R/R) acute myeloid leukemia (AML). We explored mechanisms of ivosidenib resistance in 174 patients with confirmed mIDH1 R/R AML from a phase 1 trial. Receptor tyrosine kinase (RTK) pathway mutations were associated with primary resistance to ivosidenib. Multipl

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Rozen, Esteban Javier, and Jason Matthew Shohet. "Systematic review of the receptor tyrosine kinase superfamily in neuroblastoma pathophysiology." Cancer and Metastasis Reviews 41, no. 1 (2021): 33–52. http://dx.doi.org/10.1007/s10555-021-10001-7.

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Abstract Background Neuroblastoma is a devastating disease accounting for 15% of all childhood cancer deaths. Yet, our understanding of key molecular drivers such as receptor tyrosine kinases (RTKs) in this pathology remains poorly clarified. Here, we provide a systematic analysis of the RTK superfamily in the context of neuroblastoma pathogenesis. Methods Statistical correlations for all RTK family members’ expression to neuroblastoma patient survival across 10 independent patient cohorts were annotated, synthesized, and ranked using the R2: Genomics Analysis and Visualization Platform. Gene

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Phuchareon, Janyaporn, Frank McCormick, David W. Eisele, and Osamu Tetsu. "EGFR inhibition evokes innate drug resistance in lung cancer cells by preventing Akt activity and thus inactivating Ets-1 function." Proceedings of the National Academy of Sciences 112, no. 29 (2015): E3855—E3863. http://dx.doi.org/10.1073/pnas.1510733112.

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Nonsmall cell lung cancer (NSCLC) is the leading cause of cancer death worldwide. About 14% of NSCLCs harbor mutations in epidermal growth factor receptor (EGFR). Despite remarkable progress in treatment with tyrosine kinase inhibitors (TKIs), only 5% of patients achieve tumor reduction >90%. The limited primary responses are attributed partly to drug resistance inherent in the tumor cells before therapy begins. Recent reports showed that activation of receptor tyrosine kinases (RTKs) is an important determinant of this innate drug resistance. In contrast, we demonstrate that EGFR inhibitio

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