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Relevant bibliographies by topics / Src-family kinases (SFKs)

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Academic literature on the topic 'Src-family kinases (SFKs)'

Author: Grafiati

Published: 11 March 2023

Last updated: 31 July 2025

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Journal articles on the topic "Src-family kinases (SFKs)"

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Wang, Jun, and Shougang Zhuang. "Src family kinases in chronic kidney disease." American Journal of Physiology-Renal Physiology 313, no. 3 (2017): F721—F728. http://dx.doi.org/10.1152/ajprenal.00141.2017.

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Src family kinases (SFKs) belong to nonreceptor protein tyrosine kinases and have been implicated in the regulation of numerous cellular processes, including cell proliferation, differentiation, migration and invasion, and angiogenesis. The role and mechanisms of SFKs in tumorgenesis have been extensively investigated, and some SFK inhibitors are currently under clinical trials for tumor treatment. Recent studies have also demonstrated the importance of SFKs in regulating the development of various fibrosis-related chronic diseases (e.g., idiopathic pulmonary fibrosis, liver fibrosis, renal fi

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Xiao, Xiang, Yue Yang, Baiping Mao, C. Yan Cheng, and Ya Ni. "Emerging role for SRC family kinases in junction dynamics during spermatogenesis." Reproduction 157, no. 3 (2019): R85—R94. http://dx.doi.org/10.1530/rep-18-0440.

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SRC family kinases (SFKs) are known regulators of multiple cellular events, including cell movement, differentiation, proliferation, survival and apoptosis. SFKs are expressed virtually by all mammalian cells. They are non-receptor protein kinases that phosphorylate a variety of cellular proteins on tyrosine, leading to the activation of protein targets in response to environmental stimuli. Among SFKs, SRC, YES and FYN are the ubiquitously expressed and best studied members. In fact, SRC, the prototypical SFK, was the first tyrosine kinase identified in mammalian cells. Studies have shown that

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Senis, Yotis A., Alexandra Mazharian, and Jun Mori. "Src family kinases: at the forefront of platelet activation." Blood 124, no. 13 (2014): 2013–24. http://dx.doi.org/10.1182/blood-2014-01-453134.

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Abstract Src family kinases (SFKs) play a central role in mediating the rapid response of platelets to vascular injury. They transmit activation signals from a diverse repertoire of platelet surface receptors, including the integrin αIIbβ3, the immunoreceptor tyrosine–based activation motif–containing collagen receptor complex GPVI-FcR γ-chain, and the von Willebrand factor receptor complex GPIb-IX-V, which are essential for thrombus growth and stability. Ligand-mediated clustering of these receptors triggers an increase in SFK activity and downstream tyrosine phosphorylation of enzymes, adapt

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Xiang, Binggang, Guoying Zhang, and Zhenyu Li. "Src Family Kinases Contribute to GI and Gq-Mediated Platelet Activation." Blood 118, no. 21 (2011): 5263. http://dx.doi.org/10.1182/blood.v118.21.5263.5263.

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Abstract Abstract 5263 The Src family kinases (SFKs) play an essential role in collagen- and von Willebrand factor (vWF)-mediated platelet activation. However, the role of SFKs in G protein-coupled receptor (GPCR)-mediated platelet activation is not fully understood, and little is known about the molecular mechanisms by which SFKs are activated by GPCR stimulation. Here we demonstrate that SFKs are activated by the Gq and Gi pathways, respectively and SFKs play important roles in Gq- and Gi-dependent secretion and activation. ADP induced SFK phosphorylation in wild type and Gq−/− platelets, an

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Evangelista, Virgilio, Zehra Pamuklar, Antonio Piccoli, et al. "Src family kinases mediate neutrophil adhesion to adherent platelets." Blood 109, no. 6 (2006): 2461–69. http://dx.doi.org/10.1182/blood-2006-06-029082.

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Abstract Polymorphonuclear leukocyte (PMN)–platelet interactions at sites of vascular damage contribute to local and systemic inflammation. We sought to determine the role of “outside-in” signaling by Src-family tyrosine kinases (SFKs) in the regulation of αMβ2-integrin–dependent PMN recruitment by activated platelets under (patho)physiologic conditions. Activation-dependent epitopes in β2 integrin were exposed at the contact sites between PMNs and platelets and were abolished by SFK inhibitors. PMNs from αMβ2−/−, hck−/−fgr−/−, and hck−/−fgr−/−lyn−/− mice had an impaired capacity to adhere wit

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Singh, Durgesh Kumar, Rohit Kumar Deshmukh, Praveen Kumar Narayanan, Sisinthy Shivaji, and Archana Bharadwaj Siva. "SRC family kinases in hamster spermatozoa: evidence for the presence of LCK." Reproduction 153, no. 5 (2017): 655–69. http://dx.doi.org/10.1530/rep-16-0591.

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Sperm capacitation is a prerequisite for successful fertilization. Increase in tyrosine phosphorylation is considered the hallmark of capacitation and attempts to understand its regulation are ongoing. In this regard, we attempted to study the role of SRC family kinases (SFKs) in the hamster sperm functions. Interestingly, we found the presence of the lymphocyte-specific protein tyrosine kinase, LCK, in mammalian spermatozoa and further characterized it in terms of its localization and function. LCK was found in spermatozoa of several species, and its transcript was identified in the hamster t

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Indovina, Paola, Iris Maria Forte, Francesca Pentimalli, and Antonio Giordano. "Targeting SRC Family Kinases in Mesothelioma: Time to Upgrade." Cancers 12, no. 7 (2020): 1866. http://dx.doi.org/10.3390/cancers12071866.

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Malignant mesothelioma (MM) is a deadly tumor mainly caused by exposure to asbestos. Unfortunately, no current treatment is able to change significantly the natural history of the disease, which has a poor prognosis in the majority of patients. The non-receptor tyrosine kinase SRC and other SRC family kinase (SFK) members are frequently hyperactivated in many cancer types, including MM. Several works have indeed suggested that SFKs underlie MM cell proliferation, survival, motility, and invasion, overall affecting multiple oncogenic pathways. Consistently, SFK inhibitors effectively counteract

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Bhavaraju, Kamala, Soochong Kim, and Satya P. Kunapuli. "Lyn and Fyn Kinases Positively Regulate Thromboxane Generation in Platelets." Blood 110, no. 11 (2007): 3656. http://dx.doi.org/10.1182/blood.v110.11.3656.3656.

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Abstract Src family Kinases (SFKs) are important tyrosine kinases in platelets. The family consists of 9 members (viz., Blk, Fgr, Fyn, Hck, Lck, Lyn, Src, Yes and Yrk) and many of the isoforms are expressed in platelets. SFKs are key kinases in glycoprotein (GPVI) mediated platelet activation and we have shown that these kinases play an important role in thromboxane generation. Until now, the role of specific SFKs downstream of G protein signaling in platelets is not well understood. In the present study we characterized functional roles of specific SFK members Fyn, Lyn, Lck and Src Kinases do

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Oneyama, Chitose, Takuya Iino, Kazunobu Saito, Kei Suzuki, Akira Ogawa, and Masato Okada. "Transforming Potential of Src Family Kinases Is Limited by the Cholesterol-Enriched Membrane Microdomain." Molecular and Cellular Biology 29, no. 24 (2009): 6462–72. http://dx.doi.org/10.1128/mcb.00941-09.

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ABSTRACT The upregulation of Src family kinases (SFKs) has been implicated in cancer progression, but the molecular mechanisms regulating their transforming potentials remain unclear. Here we show that the transforming ability of all SFK members is suppressed by being distributed to the cholesterol-enriched membrane microdomain. All SFKs could induce cell transformation when overexpressed in C-terminal Src kinase (Csk)-deficient fibroblasts. However, their transforming abilities varied depending on their affinity for the microdomain. c-Src and Blk, with a weak affinity for the microdomain due

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Ruiz, Ofelia S., R. Brooks Robey, Yi-Yong Qiu, et al. "Regulation of the renal Na-HCO3 cotransporter. XI. Signal transduction underlying CO2stimulation." American Journal of Physiology-Renal Physiology 277, no. 4 (1999): F580—F586. http://dx.doi.org/10.1152/ajprenal.1999.277.4.f580.

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We have previously shown that CO2 stimulation of the renal Na-HCO3 cotransporter (NBC) activity is abrogated by general inhibitors of protein tyrosine kinases. The more selective inhibitor herbimycin also blocked this effect at concentrations known to preferentially inhibit Src family kinases (SFKs). We therefore examined a role for SFKs in CO2-stimulated NBC activity. To this end, we engineered OK cells to express the COOH-terminal Src kinase (Csk), a negative regulator of SFKs. CO2 stimulated NBC activity normally in β-galactosidase-expressing and untransfected control cells. In contrast, Cs

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Dissertations / Theses on the topic "Src-family kinases (SFKs)"

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Nakanishi, Takao. "The synergistic role of ATP-dependent drug efflux pump and focal adhesion signaling pathways in vinorelbine resistance in lung cancer." Kyoto University, 2019. http://hdl.handle.net/2433/236608.

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NANI', Sara. "Signal transduction regulating formation of neutrophil extracellular traps (NETs) in response to the yeast surface component beta-glucan: role of Src-family kinases and Syk." Doctoral thesis, 2013. http://hdl.handle.net/11562/542350.

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Dopo l'attivazione, i neutrofili rilasciano fibre extracellulari o trappole extracellulari (NETs), strutture composte da cromatina e proteine granulari che legano e uccidono agenti patogeni. Tuttavia, i NETs possono contribuire a patologie sistemiche o locali, come la sepsi, la vasculite e patologie polmonari croniche come la fibrosi cistica. I meccanismi di trasduzione del segnale che regolano la formazione dei NETs sono poco conosciuti. Infatti, l'unica via finora individuata in grado di indurre la formazione dei NETs è quella basata sul modulo proteina chinasi C / intermedi reattivi dell'os

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Book chapters on the topic "Src-family kinases (SFKs)"

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Wang, Minyan, Ziyang Gong, and Zhuoan Huang. "Src family kinases (SFKs) in migraine." In Migraine Pain Management. Elsevier, 2025. http://dx.doi.org/10.1016/b978-0-443-24705-7.00009-0.

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Reports on the topic "Src-family kinases (SFKs)"

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Mohler, James L. Dependency on Src-Family Kinases (SFK) for Recurrence of Androgen-Independent Prostate Cancer. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada566915.

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