Log in

Relevant bibliographies by topics / Syk Inhibitor / Journal articles

To see the other types of publications on this topic, follow the link: Syk Inhibitor.

Journal articles on the topic 'Syk Inhibitor'

Author: Grafiati

Published: 11 March 2023

Last updated: 31 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Syk Inhibitor.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Wang, Xing, Junfang Guo, Zhongqi Ning, and Xia Wu. "Discovery of a Natural Syk Inhibitor from Chinese Medicine through a Docking-Based Virtual Screening and Biological Assay Study." Molecules 23, no. 12 (2018): 3114. http://dx.doi.org/10.3390/molecules23123114.

Full text

Abstract:

Spleen tyrosine kinase (Syk) is a critical target protein for treating immunoreceptor signalling-mediated allergies. In this study, a virtual screening of an in-house Chinese medicine database followed by biological assays was carried out to identify novel Syk inhibitors. A molecular docking method was employed to screen for compounds with potential Syk inhibitory activity. Then, an in vitro kinase inhibition assay was performed to verify the Syk inhibitory activity of the virtual screening hits. Subsequently, a β-hexosaminidase release assay was conducted to evaluate the anti-mast cell degran

APA, Harvard, Vancouver, ISO, and other styles

2

Zhao, Xiaoxian, Andrew E. Schade, and Eric Hsi. "Distinct Role of Src Family Kinase Inhibitors in Burkitt Lymphoma Cells Vs. Diffuse Large B-Cell Lymphoma Cells." Blood 112, no. 11 (2008): 3765. http://dx.doi.org/10.1182/blood.v112.11.3765.3765.

Full text

Abstract:

Abstract Introduction: The Non-Hodgkin lymphomas (NHLs) are a heterogeneous group of malignancies, with approximately 85% of NHL belonging to the B-cell lineage. Src family kinases (SFKs) are non-receptor intracellular tyrosine kinases which are important in the regulation of multiple signaling pathways including cell proliferation, tumor invasiveness, angiogenesis and apoptosis. Syk is another predominant tyrosine kinase expressed in B-cell lines in addition to SFKs. We attempted to correlate SFK and Syk inhibitor efficacy with the presence of phospho-SFK or phospho-Syk in lymphoma cell lines

APA, Harvard, Vancouver, ISO, and other styles

3

Buchner, Maike, Simon Fuchs, Gabriele Prinz, et al. "Spleen Tyrosine Kinase (SYK) Is Overexpressed and Represents a Potential Therapeutic Target in Chronic Lymphocytic Leukemia." Blood 112, no. 11 (2008): 543. http://dx.doi.org/10.1182/blood.v112.11.543.543.

Full text

Abstract:

Abstract B cell chronic lymphocytic leukemia (CLL), the most prevalent B cell malignancy in adults, is characterized by expansion of monoclonal mature B lymphocytes. Despite advances in treatment, the disease remains incurable warranting further efforts to identify novel molecular targets in CLL. B cell receptor (BCR) signaling contributes to apoptosis resistance in CLL limiting the efficacy of therapeutic approaches. In this study we investigated the expression of spleen tyrosine kinase (SYK), a key component of the BCR signaling pathway, in CLL and its role in apoptosis. Gene expression prof

APA, Harvard, Vancouver, ISO, and other styles

4

Bertoni, Francesco, Andrea Rinaldi, Anna Sasso, et al. "In Vitro Activity of SYK and BCR-ABL Inhibitors in Aggressive Lymphomas." Blood 108, no. 11 (2006): 2520. http://dx.doi.org/10.1182/blood.v108.11.2520.2520.

Full text

Abstract:

Abstract The B cell receptor tyrosine kinase SYK is a critical component of the B-cell receptor signalling pathway in normal B cells. We have recently reported that SYK is amplified and over-expressed in mantle cell lymphoma (MCL) and that the growth of MCL and diffuse large B cell lymphoma (DLBCL) cell lines over-expressing SYK is inhibited by piceatannol, a known SYK inhibitor (Bertoni et al, ASH 2005; Rinaldi et al, BJH 2006). Others have reported important SYK expression in splenic marginal zone B cell lymphomas, in DLBCL and peripheral T cell lymphomas (PTCL) (Ruiz-Ballesteros et al, 2005

APA, Harvard, Vancouver, ISO, and other styles

5

Huang, Duen-Yi, Wei-Yu Chen, Chi-Long Chen, Nan-Lin Wu, and Wan-Wan Lin. "Synergistic Anti-Tumour Effect of Syk Inhibitor and Olaparib in Squamous Cell Carcinoma: Roles of Syk in EGFR Signalling and PARP1 Activation." Cancers 12, no. 2 (2020): 489. http://dx.doi.org/10.3390/cancers12020489.

Full text

Abstract:

Syk is a non-receptor tyrosine kinase involved in the signalling of immunoreceptors and growth factor receptors. Previously, we reported that Syk mediates epidermal growth factor receptor (EGFR) signalling and plays a negative role in the terminal differentiation of keratinocytes. To understand whether Syk is a potential therapeutic target of cancer cells, we further elucidated the role of Syk in disease progression of squamous cell carcinoma (SCC), which is highly associated with EGFR overactivation, and determined the combined effects of Syk and PARP1 inhibitors on SCC viability. We found th

APA, Harvard, Vancouver, ISO, and other styles

6

Coates, Matthew S., Eric W. F. W. Alton, Garth W. Rapeport, Jane C. Davies, and Kazuhiro Ito. "Pseudomonas aeruginosa induces p38MAP kinase-dependent IL-6 and CXCL8 release from bronchial epithelial cells via a Syk kinase pathway." PLOS ONE 16, no. 2 (2021): e0246050. http://dx.doi.org/10.1371/journal.pone.0246050.

Full text

Abstract:

Pseudomonas aeruginosa (Pa) infection is a major cause of airway inflammation in immunocompromised and cystic fibrosis (CF) patients. Mitogen-activated protein (MAP) and tyrosine kinases are integral to inflammatory responses and are therefore potential targets for novel anti-inflammatory therapies. We have determined the involvement of specific kinases in Pa-induced inflammation. The effects of kinase inhibitors against p38MAPK, MEK 1/2, JNK 1/2, Syk or c-Src, a combination of a p38MAPK with Syk inhibitor, or a novel narrow spectrum kinase inhibitor (NSKI), were evaluated against the release

APA, Harvard, Vancouver, ISO, and other styles

7

Makhoul, Stephanie, Stephanie Dorschel, Stepan Gambaryan, Ulrich Walter, and Kerstin Jurk. "Feedback Regulation of Syk by Protein Kinase C in Human Platelets." International Journal of Molecular Sciences 21, no. 1 (2019): 176. http://dx.doi.org/10.3390/ijms21010176.

Full text

Abstract:

The spleen tyrosine kinase (Syk) is essential for immunoreceptor tyrosine-based activation motif (ITAM)-dependent platelet activation, and it is stimulated by Src-family kinase (SFK)-/Syk-mediated phosphorylation of Y352 (interdomain-B) and Y525/526 (kinase domain). Additional sites for Syk phosphorylation and protein interactions are known but remain elusive. Since Syk S297 phosphorylation (interdomain-B) was detected in platelets, we hypothesized that this phosphorylation site regulates Syk activity via protein kinase C (PKC)-and cyclic adenosine monophosphate (cAMP)-dependent pathways. ADP,

APA, Harvard, Vancouver, ISO, and other styles

8

Issara-Amphorn, Jiraphorn, Naraporn Somboonna, Prapaporn Pisitkun, Nattiya Hirankarn, and Asada Leelahavanichkul. "Syk inhibitor attenuates inflammation in lupus mice from FcgRIIb deficiency but not in pristane induction: the influence of lupus pathogenesis on the therapeutic effect." Lupus 29, no. 10 (2020): 1248–62. http://dx.doi.org/10.1177/0961203320941106.

Full text

Abstract:

Macrophages are responsible for the recognition of pathogen molecules. The downstream signalling of the innate immune responses against pathogen molecules, lipopolysaccharide (LPS) and (1→3)-β-D-glucan (BG), and the adaptive immune response to antibodies, Fc gamma receptor (FcgR), is spleen tyrosine kinase (Syk). Because pathogen molecules and antibodies could be presented in lupus, impact of Syk and macrophages in lupus is explored. FcgR-IIb deficient (FcgRIIb-/-) mice, a model of inhibitory signalling loss, at 40 weeks old, but not pristane mice (a chemical induction lupus model) demonstrate

APA, Harvard, Vancouver, ISO, and other styles

9

Getz, Todd M., Bhanu Manne, Lorena Buitrago, Yingying Mao, and Satya P. Kunapuli. "Dextran sulphate induces fibrinogen receptor activation through a novel Syk-independent PI-3 kinase-mediated tyrosine kinase pathway in platelets." Thrombosis and Haemostasis 109, no. 06 (2013): 1131–40. http://dx.doi.org/10.1160/th12-09-0645.

Full text

Abstract:

SummaryIn our attempt to find a physiological agonist that activates PAR3 receptors, we screened several coagulation proteases using PAR4 null platelets. We observed that FXIIa and heat inactivated FXIIa, but not FXII, caused platelet aggregation. We have identified a contaminant activating factor in FXIIa preparation as dextran sulfate (DxS), which caused aggregation of both human and mouse platelets. DxS-induced platelet aggregation was unaffected by YM254890, a Gq inhibitor, but abolished by pan-Src family kinase (SFK) inhibitor PP2, suggesting a role for SFKs in this pathway. However, DxS-

APA, Harvard, Vancouver, ISO, and other styles

10

Kiliszek, Przemyslaw, Maciej Szydlowski, Tomasz Sewastianik, et al. "FOXO1 Activation Is an Effector of SYK and AKT Inhibition in Tonic BCR Signal-Dependent Diffuse Large B-Cell Lymphomas." Blood 126, no. 23 (2015): 314. http://dx.doi.org/10.1182/blood.v126.23.314.314.

Full text

Abstract:

Abstract Introduction: In normal B lymphocytes, B-cell receptor (BCR)-induced activation of PI3K-AKT kinases and subsequent inactivation of FOXO1 is a critical pro-survival component of tonic BCR signaling. In murine models, conditional deletion of FOXO1 protected quiescent peripheral B cells from apoptosis mediated by inducible loss of the BCR, demonstrating that PI3K-AKT-FOXO1 axis plays a central role in B-cell homeostasis. Disruption of the BCR signaling by SYK inhibitor leads also to the apoptosis of BCR-dependent DLBCLs, at least in part via a mechanism involving decreased activity of PI

APA, Harvard, Vancouver, ISO, and other styles

11

Issara-Amphorn, Jiraphorn, Wiwat Chancharoenthana, Peerapat Visitchanakun, and Asada Leelahavanichkul. "Syk Inhibitor Attenuates Polymicrobial Sepsis in FcgRIIb-Deficient Lupus Mouse Model, the Impact of Lupus Characteristics in Sepsis." Journal of Innate Immunity 12, no. 6 (2020): 461–79. http://dx.doi.org/10.1159/000509111.

Full text

Abstract:

The impact of spleen tyrosine kinase (Syk) signaling might be prominent in lupus because (i) Syk is a shared downstream signaling molecule among circulating immune complex, LPS, and (1→3)-β-D-glucan (BG), and (ii) all of these factors are detectable in the serum of Fc gamma receptor IIb-deficient (FcgRIIb<sup>−/−</sup>) mice with sepsis. As a proof of concept study, we activated macrophages with BG combined with LPS (BG + LPS). We found that BG + LPS predominantly upregulated Syk expression and proinflammatory cytokines in FcgRIIb<sup>−/−</sup> macrophages compared with

APA, Harvard, Vancouver, ISO, and other styles

12

Yang, Na, Wei Deng, Qiaoling Sun, et al. "HMPL-523, a Novel SYK Inhibitor Showed Anti-Tumor Activities In Vitro and In Vivo." Blood 128, no. 22 (2016): 3970. http://dx.doi.org/10.1182/blood.v128.22.3970.3970.

Full text

Abstract:

Abstract Introduction: Spleen Tyrosine Kinase (SYK), a non-receptor type of tyrosine kinase, is a member of Syk/ZAP70 tyrosine kinase family. It plays a pivotal role in the regulation of B-cell receptor (BCR) signal pathway, which regulates proliferation, differentiation and survival of B lymphocytes. The abnormal activation of BCR singling is closely related to transformation and development of B cell lymphoma. Targeting BCR downstream molecules, such as Bruton' tyrosine kinase (BTK) and phosphoinositide-3-kinase δ (PI3Kδ) has emerged as new therapeutic approaches and inhibitors of BTK and PI

APA, Harvard, Vancouver, ISO, and other styles

13

Han, Yingjie, Frank Y. Ma, Julie Di Paolo, and David J. Nikolic-Paterson. "An inhibitor of spleen tyrosine kinase suppresses experimental crescentic glomerulonephritis." International Journal of Immunopathology and Pharmacology 32 (January 1, 2018): 205873841878340. http://dx.doi.org/10.1177/2058738418783404.

Full text

Abstract:

Non-selective inhibitors of spleen tyrosine kinase (SYK) efficiently suppress disease in T cell-dependent models of crescentic glomerulonephritis. However, the therapeutic potential of selective SYK inhibitors in this disease has not been established. In addition, we lack knowledge regarding SYK expression in non-myeloid cells in glomerulonephritis. We addressed these two issues in a rat model of nephrotoxic serum nephritis (NTN) using a SYK inhibitor, GS-492429. Disease was induced in Sprague-Dawley rats (Study 1) or Wistar-Kyoto (WKY) rats (Study 2) by immunization with sheep IgG and adminis

APA, Harvard, Vancouver, ISO, and other styles

14

Saturno, Grazia, Michele Modugno, Paolo Orsini, et al. "Abstract 4036: NMS-0963 is a novel potent, selective and orally available Syk inhibitor with promising preclinical activity in diffuse large B-cell lymphoma." Cancer Research 83, no. 7_Supplement (2023): 4036. http://dx.doi.org/10.1158/1538-7445.am2023-4036.

Full text

Abstract:

Abstract The B-cell receptor (BCR) is a key survival molecule for normal B cells and for most B-cell malignancies, such as Chronic Lymphocytic Leukaemia (CLL) and Non-Hodgkin’s Lymphomas (NHL) including Diffuse Large B-cell Lymphomas (DLBCL). Small molecule inhibitors of key signaling kinases involved in the BCR pathway, such as the Btk inhibitor ibrutinib and the PI3Kdelta inhibitor idelalisib, have already demonstrated significant clinical activity. Spleen tyrosine kinase (Syk) is a non-receptor cytoplasmic tyrosine kinase that plays a fundamental role in BCR signaling initiation thus repres

APA, Harvard, Vancouver, ISO, and other styles

15

Pamuk, Omer Nuri, Peter H. Lapchak, Poonam Rani, Polly Pine, Jurandir J. Dalle Lucca, and George C. Tsokos. "Spleen tyrosine kinase inhibition prevents tissue damage after ischemia-reperfusion." American Journal of Physiology-Gastrointestinal and Liver Physiology 299, no. 2 (2010): G391—G399. http://dx.doi.org/10.1152/ajpgi.00198.2010.

Full text

Abstract:

Reperfusion injury to tissue following an ischemic event occurs as a consequence of an acute inflammatory response that can cause significant morbidity and mortality. Components of both the innate (complement, immunoglobulin, monocytes, and neutrophils) and adaptive (B and T lymphocytes) immune systems have been demonstrated to mediate tissue injury. Spleen tyrosine kinase (Syk) is responsible for membrane-mediated signaling in various cell types including B lymphocytes, macrophages, and T cells. We investigated the ability of a small drug Syk inhibitor, R788, to protect mice against mesenteri

APA, Harvard, Vancouver, ISO, and other styles

16

Abraham, Shaji, Carol T. Dangelmaier, Yuhang Zhou та ін. "Syk Is Regulated Downstream Of FcγRIIA In Platelets By Transient Tyrosine Phosphorylation and Ubiquitylation". Blood 122, № 21 (2013): 4737. http://dx.doi.org/10.1182/blood.v122.21.4737.4737.

Full text

Abstract:

Platelet FcγRIIA contributes to the pathophysiology of heparin-induced thrombocytopenia (HIT) and other immune-mediated thrombocytopenia and thrombosis syndromes. Activation of FcγRIIA results in tyrosine phosphorylation of Syk in human platelets, but little is known about ubiquitylation of Syk. Protein ubiquitylation has been shown to regulate physiological and pathological cellular processes by regulating signaling networks. In the Platelet RNA and Expression-1 (PRAX1) study, we studied platelets from 154 healthy subjects and identified increased expression of mRNAs encoding proteins involve

APA, Harvard, Vancouver, ISO, and other styles

17

Biagioli, Michele, Andrea Mencarelli, Adriana Carino, et al. "Genetic and Pharmacological Dissection of the Role of Spleen Tyrosine Kinase (Syk) in Intestinal Inflammation and Immune Dysfunction in Inflammatory Bowel Diseases." Inflammatory Bowel Diseases 24, no. 1 (2017): 123–35. http://dx.doi.org/10.1093/ibd/izx031.

Full text

Abstract:

Abstract Background The DNAX adaptor protein 12 (DAP12) is a transmembrane adaptor molecule that signals through the activation of Syk (Spleen Tyrosine Kinase) in myeloid cells. The purpose of this study is to investigate the role of DAP12 and Syk pathways in inflammatory bowel diseases (IBDs). Methods DAP12 deficient and DAP12 transgenic, overexpressing an increased amount of DAP12, mice and Syk deficient mice in the C57/BL6 background were used for these studies. Colitis was induced by administering mice with dextran sulfate sodium (DSS), in drinking water, or 2,4,6-trinitrobenzene sulfonic

APA, Harvard, Vancouver, ISO, and other styles

18

Sender, Sina, Ahmad Wael Sultan, Daniel Palmer, et al. "Evaluation of the Synergistic Potential of Simultaneous Pan- or Isoform-Specific BET and SYK Inhibition in B-Cell Lymphoma: An In Vitro Approach." Cancers 14, no. 19 (2022): 4691. http://dx.doi.org/10.3390/cancers14194691.

Full text

Abstract:

Background: Both bromodomain and extra-terminal domain (BET) proteins and spleen tyrosine kinase (SYK) represent promising targets in diffuse large B-cell (DLBCL) and Burkitt’s lymphoma (BL). We evaluated the anti-lymphoma activity of the isoform-specific bivalent BET inhibitor AZD5153 (AZD) and the pan-BET inhibitor I-BET151 (I-BET) as single agents and in combination with SYK inhibitor Entospletinib (Ento) in vitro. Methods: The effect of the single agents on cell proliferation and metabolic activity was evaluated in two DLBCL and two BL cell lines. Proliferation, metabolic activity, apoptos

APA, Harvard, Vancouver, ISO, and other styles

19

Tümmler, Conny, Gianina Dumitriu, Malin Wickström, et al. "SYK Inhibition Potentiates the Effect of Chemotherapeutic Drugs on Neuroblastoma Cells in Vitro." Cancers 11, no. 2 (2019): 202. http://dx.doi.org/10.3390/cancers11020202.

Full text

Abstract:

Neuroblastoma is a malignancy arising from the developing sympathetic nervous system and the most common and deadly cancer of infancy. New therapies are needed to improve the prognosis for high-risk patients and to reduce toxicity and late effects. Spleen tyrosine kinase (SYK) has previously been identified as a promising drug target in various inflammatory diseases and cancers but has so far not been extensively studied as a potential therapeutic target in neuroblastoma. In this study, we observed elevated SYK gene expression in neuroblastoma compared to neural crest and benign neurofibroma.

APA, Harvard, Vancouver, ISO, and other styles

20

Hoellenriegel, Julia, Greg Coffey, Uma Sinha, et al. "Spleen Tyrosine Kinase (Syk) Inhibitors Block B Cell Receptor Signaling and Survival In Chronic Lymphocytic Leukemia." Blood 116, no. 21 (2010): 3604. http://dx.doi.org/10.1182/blood.v116.21.3604.3604.

Full text

Abstract:

Abstract Abstract 3604 B cell antigen receptor (BCR) signaling is increasingly recognized as a key factor promoting clonal expansion in various B cell malignancies, such as diffuse large B cell lymphoma and CLL. Engagement of the BCR receptor activates Syk, which leads to a number of downstream events that promote cell survival and growth. Therefore, inhibition of Syk represents a novel therapeutic approach in CLL. Another Syk inhibitor (fostamatinib disodium/R788) has clinical activity in patients with CLL (Blood 115: 2570, 2010). R788 is a relatively selective Syk inhibitor, but also display

APA, Harvard, Vancouver, ISO, and other styles

21

Zhou, Zhou, Francisca C. Gushiken, Angela Bergeron, et al. "STAT3 Regulates Collagen-Induced Platelet Aggregation Independent of Its Transcription Factor Activity." Blood 116, no. 21 (2010): 157. http://dx.doi.org/10.1182/blood.v116.21.157.157.

Full text

Abstract:

Abstract Abstract 157 Signal Transducer and Activator of Transcription 3 (STAT3) serves as a transcription factor activated by cytokine-induced intracellular signals, which are critical in megakaryopoiesis. This signaling pathway may also be active in anucleated platelets that are primed by proinflammatory cytokines, suggesting that STAT3 plays a role in platelet hyperactivity associated with inflammation. We have recently found that three different classes of STAT3 inhibitors each selectively inhibited collagen-induced aggregation of human platelets by ∼50%. They also blocked thrombus formati

APA, Harvard, Vancouver, ISO, and other styles

22

Woulfe, Donna S. "A Syk inhibitor for sick platelets?" Blood 113, no. 14 (2009): 3133–34. http://dx.doi.org/10.1182/blood-2009-01-199778.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Hahn, Cynthia K., Kenneth N. Ross, Rose M. Kakoza, et al. "Syk Is a New Target for AML Differentiation." Blood 110, no. 11 (2007): 209. http://dx.doi.org/10.1182/blood.v110.11.209.209.

Full text

Abstract:

Abstract One of the challenges of phenotype-based small molecule screening has been the difficulty of protein target identification for newly discovered compounds. For example, we previously performed a gene expression-based small molecule library screen, which identified gefitinib, an epidermal growth factor receptor (EGFR) inhibitor, as an inducer of acute myeloid leukemia (AML) differentiation in cell lines and primary patient cells. Neither EGFR transcript nor protein is expressed in the tested AML cell lines, thus precluding inhibition of this kinase as the mechanism of AML differentiatio

APA, Harvard, Vancouver, ISO, and other styles

24

Chen, Liguang, George Chen, Jessie-Farah Fecteau, et al. "Highly Specific Inhibitor for Syk Induces Chronic Lymphocytic Leukemia Cell Apoptosis,." Blood 118, no. 21 (2011): 3875. http://dx.doi.org/10.1182/blood.v118.21.3875.3875.

Full text

Abstract:

Abstract Abstract 3875 The antibodies expressed by CLL cells are highly selected, implicating a role for antigen in the pathogenesis of this disease. The B-cell receptor (BCR) for antigen may become engaged by microbial or self-antigens to induce activation of downstream adapter/signaling molecules. This, either alone or in concert with activation of other receptors, can induce CLL-cell expression of genes encoding proteins involved in cell survival or proliferation, e.g. c-MYC, potentially enhancing the tendency for disease progression. Our prior studies found that ZAP-70 in CLL cells enhance

APA, Harvard, Vancouver, ISO, and other styles

25

Lin, Yipeng. "Kinase inhibitor therapies for Chronic lymphocytic leukaemia (CLL): SYK, BTK and PI3K inhibitors." Highlights in Science, Engineering and Technology 19 (November 17, 2022): 30–35. http://dx.doi.org/10.54097/hset.v19i.2691.

Full text

Abstract:

Chronic lymphocytic leukaemia (CLL) is a prevalent tumor disease in developed countries, and related therapies have been designed. However, CLL is still incurable. Chemoimmunotherapy is effective in inhibiting the proliferation of CLL cells, but nonspecific treatment can affect the growth of other immune cells. Kinase inhibitors are considered to be effective treatments for CLL as their anti-proliferation effects, and currently, popular kinase inhibitor therapies include SYK, BTK, and PI3K inhibitor therapy. PI3K is characterized by high efficiency and low side effects compared with the other

APA, Harvard, Vancouver, ISO, and other styles

26

Pokrovskaya, Irina D., Kelly K. Ball, Michael W. Webb, et al. "Contrasting Effects of Platelet GPVI Deletion Versus Syk Inhibition on Mouse Jugular Vein Puncture Wound Structure." International Journal of Molecular Sciences 26, no. 9 (2025): 4294. https://doi.org/10.3390/ijms26094294.

Full text

Abstract:

Platelet glycoprotein (GP)VI is a transmembrane protein that was originally characterized as a collagen receptor supporting platelet adhesion and activation through its association with the Fc receptor γ-chain (FcRγ). The FcRγ subunit contains immunoreceptor tyrosine-based activation motifs (ITAMs) that recruit and activate Syk (spleen tyrosine kinase), a key player in intracellular signaling pathways. The absence or dysfunction of GPVI produces a mild bleeding defect in humans like the impaired hemostasis reported in the murine knockout. Here, we took an ultrastructure approach to examine the

APA, Harvard, Vancouver, ISO, and other styles

27

Perrella, Gina, Samantha J. Montague, Helena C. Brown, et al. "Role of Tyrosine Kinase Syk in Thrombus Stabilisation at High Shear." International Journal of Molecular Sciences 23, no. 1 (2022): 493. http://dx.doi.org/10.3390/ijms23010493.

Full text

Abstract:

Understanding the pathways involved in the formation and stability of the core and shell regions of a platelet-rich arterial thrombus may result in new ways to treat arterial thrombosis. The distinguishing feature between these two regions is the absence of fibrin in the shell which indicates that in vitro flow-based assays over thrombogenic surfaces, in the absence of coagulation, can be used to resemble this region. In this study, we have investigated the contribution of Syk tyrosine kinase in the stability of platelet aggregates (or thrombi) formed on collagen or atherosclerotic plaque homo

APA, Harvard, Vancouver, ISO, and other styles

28

Chen, Linfeng, Przemyslaw Juszczynski, Yasumichi Hitoshi, Wen Chen, Jeffery L. Kutok, and Margaret A. Shipp. "Tonic B-Cell Receptor Signaling Promotes the Survival of Diffuse Large B-Cell Lymphomas: Identification of SYK as a Rational Treatment Target." Blood 108, no. 11 (2006): 226. http://dx.doi.org/10.1182/blood.v108.11.226.226.

Full text

Abstract:

Abstract The role of BCR-mediated survival signals in diffuse large B-cell lymphoma (DLBCL) remains undefined. B-cell antigen receptor (BCR) signaling induces receptor oligomerization and Ig alpha/beta ITAM phosphorylation. Thereafter, the protein tyrosine kinase (PTK) SYK is recruited and activated, initiating downstream events and amplifying the original BCR signal. Recent studies indicate that BCRs also transmit low-level survival signals in the absence of receptor engagement and highlight the critical role of SYK in this “tonic” BCR signaling. We recently found that SYK is a major substrat

APA, Harvard, Vancouver, ISO, and other styles

29

Buchner, Maike, Constance Baer, Gabriele Prinz, et al. "Spleen tyrosine kinase inhibition prevents chemokine- and integrin-mediated stromal protective effects in chronic lymphocytic leukemia." Blood 115, no. 22 (2010): 4497–506. http://dx.doi.org/10.1182/blood-2009-07-233692.

Full text

Abstract:

Abstract The microenvironment provides essential growth and survival signals to chronic lymphocytic leukemia (CLL) cells and contributes to their resistance to cytotoxic agents. Pharmacologic inhibition of spleen tyrosine kinase (SYK), a key mediator of B-cell receptor (BCR) signaling, induces apoptosis in primary CLL cells and prevents stroma contact-mediated cell survival. This report demonstrates a role of SYK in molecularly defined pathways that mediate the CLL-microenvironmental crosstalk independent from the BCR. Chemokine and integrin stimulation induced SYK phosphorylation, SYK-depende

APA, Harvard, Vancouver, ISO, and other styles

30

Balaian, Larissa, and Edward D. Ball. "The Anti-Proliferative Effect of Immunotoxin Gemtuzimab Ozogamycin (GO) (Mylotarg) to Acute Myeloid Leukemia (AML) Cells Is Associated with the Level of Protein Kinase Syk Exspression." Blood 104, no. 11 (2004): 96. http://dx.doi.org/10.1182/blood.v104.11.96.96.

Full text

Abstract:

Abstract AML cells express the cell surface antigen CD33 that serves as a down-regulator of cell growth. Anti-CD33 monoclonal antibody (mAb) coupled to a toxin is a licensed drug for the treatment of relapsed AML (Mylotarg). Syk is not only an essential element in several cascades coupling antigen receptors to cell responses, but also SYK is a tumor suppressor gene. Silencing of SYK by hypermethylation results in absence of Syk expression and unresponsiveness of tumor cells to various treatments.. Earlier we demonstrated that about 30% of the AML samples were Syk-negative and the response of l

APA, Harvard, Vancouver, ISO, and other styles

31

Abraham, Shaji, Leonard C. Edelstein, Chad A. Shaw та ін. "Platelet FcγRIIA Signaling Results in Ubiquitination and Cellular Translocation of Activated Syk". Blood 124, № 21 (2014): 2761. http://dx.doi.org/10.1182/blood.v124.21.2761.2761.

Full text

Abstract:

Abstract Platelet FcγRIIA is central to the pathophysiology of immune-mediated thrombocytopenia and thrombosis syndromes, such as heparin-induced thrombocytopenia (HIT). FcγRIIA is also the major transmembrane signaling adapter for αIIbβ3 outside-in signaling. In HIT, antibody to heparin/PF4 is necessary but not sufficient for disease to occur. Inter-individual variation in platelet activation via FcγRIIA contributes to HIT risk, but the molecular basis for the variation is incompletely understood. In our PRAX1 study of platelet reactivity and RNA expression (Edelstein, Nature Med 2013; Simon,

APA, Harvard, Vancouver, ISO, and other styles

32

Patou, Joke, Gabriele Holtappels, Karen Affleck, Paul van Cauwenberge, and Claus Bachert. "Syk-kinase inhibition prevents mast cell activation in nasal polyps." Rhinology journal 49, no. 1 (2011): 100–106. http://dx.doi.org/10.4193/rhino09.147.

Full text

Abstract:

Background: Mast cells are crucial effector cells in the allergic cascade. The cross-linking of the high affinity IgE receptor (FcεRI) activates mast cells and basophils. Spleen tyrosine kinase (Syk) is positioned upstream of the IgE receptor signal transducing pathway and may represent an important target for the treatment of nasal inflammatory diseases. Objective: We measured effects of a specific Syk inhibitor in the release of mast cell mediators in human cord blood-derived mast cells (CBDMCs) (in-vitro) and in human nasal tissue (ex-vivo). Methods: Surgical samples were collected from pat

APA, Harvard, Vancouver, ISO, and other styles

33

Storrie, Brian, Irina D. Pokrovskaya, Kelly K. Ball, and Michael W. Webb. "Differential Effects of GPVI Deletion and SYK Inhibition on Thrombus Organization and Platelet Adhesion in a Murine Jugular Puncture Wound Model." Blood 144, Supplement 1 (2024): 5421. https://doi.org/10.1182/blood-2024-211808.

Full text

Abstract:

Essential Points GPVI is the major collagen receptor in platelets as well as a receptor for fibrinogen/fibrin and signals intracellularly by activating SYK kinase.Deletion of GPVI in contrast to SYK inhibitor treatment has a mild but significant effect on jugular vein puncture wound bleeding cessation in the murine model. The SYK inhibitor was used at a concentration sufficient to inhibit ferric chloride induced occlusive clotting.Deletion of either GPVI or SYK inhibition inhibits the induction of a high platelet activation state at the collagen/thrombus interface and results in a thinning of

APA, Harvard, Vancouver, ISO, and other styles

34

Cheng, Shuhua, Greg Coffey, X. Hannah Zhang, et al. "SYK inhibition and response prediction in diffuse large B-cell lymphoma." Blood 118, no. 24 (2011): 6342–52. http://dx.doi.org/10.1182/blood-2011-02-333773.

Full text

Abstract:

Abstract Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma, and the role of SYK in its pathogenesis is not completely understood. Using tissue microarray, we demonstrated for the first time that SYK protein is activated in 27 of 61 (44%) primary human DLBCL tissues. Among DLBCL cell lines, 7 were sensitive and 3 were resistant to a highly specific SYK inhibitor, PRT060318. In sensitive DLBCL cells, SYK inhibition blocked the G1-S transition and caused cell-cycle arrest. This effect was reproduced by genetic reduction of SYK using siRNA. A detailed analysis o

APA, Harvard, Vancouver, ISO, and other styles

35

Raeder, Evelin M. B., Pamela J. Mansfield, Vania Hinkovska-Galcheva, James A. Shayman, and Laurence A. Boxer. "Syk Activation Initiates Downstream Signaling Events During Human Polymorphonuclear Leukocyte Phagocytosis." Journal of Immunology 163, no. 12 (1999): 6785–93. http://dx.doi.org/10.4049/jimmunol.163.12.6785.

Full text

Abstract:

Abstract We investigated the requirement for Syk activation to initiate downstream signaling events during polymorphonuclear leukocyte (PMN) phagocytosis of Ab-coated erythrocytes (EIgG). When PMN were challenged with EIgG, Syk phosphorylation increased in a time-dependent manner, paralleling the response of PMN phagocytosis. Pretreatment of PMN with piceatannol, a Syk-selective inhibitor, blocked EIgG phagocytosis and Syk phosphorylation. We found that piceatannol inhibited protein kinase Cδ (PKCδ) and Raf-1 translocation from cytosol to plasma membrane by &gt;90%. Extracellular signal-re

APA, Harvard, Vancouver, ISO, and other styles

36

Kuroda, Etsushi, Keiichi Ohata, Cevayir Coban, and Ken Ishii. "Particulates induce macrophages to produce lipid mediators via the Syk activation. (172.25)." Journal of Immunology 188, no. 1_Supplement (2012): 172.25. http://dx.doi.org/10.4049/jimmunol.188.supp.172.25.

Full text

Abstract:

Abstract Some particulate such as silica crystal (silica), aluminum salts (alum) and monosodium urate (MSU) can stimulate the innate immune system to induce inflammatory responses. Recently, we found that silica and alum induce macrophages to produce both IL-1β and lipid mediator prostaglandin E2 (PGE2). We also indicated that particulate-induced PGE2 is involved in the production of IgE in vivo. However, the underlying mechanisms involved in the induction of PGE2 by particulate remain to be elucidated. In this study, we show that Syk plays an important role in particulate-induced PGE2 product

APA, Harvard, Vancouver, ISO, and other styles

37

Yang, Won Seok, Joon-Seok Kim, Nam Jeong Han, Mee Jeong Lee, and Su-Kil Park. "Toll-Like Receptor 4/Spleen Tyrosine Kinase Complex in High Glucose Signal Transduction of Proximal Tubular Epithelial Cells." Cellular Physiology and Biochemistry 35, no. 6 (2015): 2309–19. http://dx.doi.org/10.1159/000374034.

Full text

Abstract:

Background/Aims: High glucose activates spleen tyrosine kinase (Syk) in human proximal tubular epithelial cells (HK-2 cells), which leads to NF-κB activation and transforming growth factor-ß1 (TGF-ß1) production. We explored the signal transduction pathway from high glucose to Syk activation. Methods: The pathway was evaluated by siRNA transfection, immunoprecipitation and Western blot. Results: High glucose stimulated Syk activation within 10 min. Depletion of toll-like receptor 4 (TLR4) attenuated high glucose-induced Syk activation, NF-κB p65 nuclear translocation, and TGF-ß1 production. In

APA, Harvard, Vancouver, ISO, and other styles

38

YAMAOKA, Kunihiro, Kazuyoshi SAITO, and Yoshiya TANAKA. "4. Drugs Targeting Intracellular Molecule: JAK Inhibitor and Syk Inhibitor." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 44, no. 1 (2013): 23–27. http://dx.doi.org/10.3999/jscpt.44.23.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Rohila, Deepak, In Hwan Park, Timothy Pham, et al. "Abstract 3246: Targeting Syk reprograms tumor-associated macrophages and enhances responses to immune checkpoint blockade and radiation therapy in high-risk neuroblastoma." Cancer Research 83, no. 7_Supplement (2023): 3246. http://dx.doi.org/10.1158/1538-7445.am2023-3246.

Full text

Abstract:

Abstract Neuroblastoma (NB) is the most common extracranial solid malignancy in children. As leading regulators of inflammation and tumor progression, tumor associated macrophages (TAMs) have gained major interest as immunotherapeutic targets in NB. Hence targeting or “re-educating” tumorigenic macrophages towards an immunostimulatory phenotype might improve responses to immunotherapy in this childhood cancer. Spleen tyrosine kinase (Syk) has recently been identified by our group as a novel immune-oncology target. We found that Syk is abundantly present in TAMs infiltrated in MYCN and non-MYCN

APA, Harvard, Vancouver, ISO, and other styles

40

Flynn, Ryan, Jessica L. Allen, Leo Luznik, et al. "Targeting Syk-activated B cells in murine and human chronic graft-versus-host disease." Blood 125, no. 26 (2015): 4085–94. http://dx.doi.org/10.1182/blood-2014-08-595470.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Uckun, Fatih M., Sanjive Qazi, Ingrid Cely, et al. "Nanoscale liposomal formulation of a SYK P-site inhibitor against B-precursor leukemia." Blood 121, no. 21 (2013): 4348–54. http://dx.doi.org/10.1182/blood-2012-11-470633.

Full text

Abstract:

Key Points SYK is a suitable molecular target for nanotechnology-enabled therapy against ALL. Nanoscale liposomal formulation of SYK inhibitor C61 displayed a promising preclinical profile as an antileukemic drug candidate.

APA, Harvard, Vancouver, ISO, and other styles

42

Spurgeon, Stephen, Luke B. Fletcher, Jeffrey W. Tyner, et al. "P505-15, a Highly Selective SYK Inhibitor, Shows Significant Activity In Primary CLL Cells and Is Synergistic with Fludarabine at Low Concentrations." Blood 116, no. 21 (2010): 2839. http://dx.doi.org/10.1182/blood.v116.21.2839.2839.

Full text

Abstract:

Abstract Abstract 2839 Background: Chronic lymphocytic leukemia (CLL) is the most common leukemia in the Western World. Despite significant progress, CLL remains incurable so novel therapies are needed. Recent studies have highlighted the importance of B-cell receptor (BCR) associated kinases in the pathogenesis of B cell malignancies and as potential therapeutic targets. Spleen tyrosine kinase (SYK) is of particular interest as its activation results in enhanced proliferation and survival of B-cells. Analysis of non-Hodgkins lymphoma (NHL) cell lines and primary chronic lymphocytic leukemia (

APA, Harvard, Vancouver, ISO, and other styles

43

Li, Shirong, Jing Fu, Jing Wu, Markus Y. Mapara, and Suzanne Lentzsch. "SYK-Inhibitor Bay 61-3606 Induces Cell Cycle Arrest and Apoptosis in Multiple Myeloma Cells Independent of SYK Inhibitory Effects but Via Degradation of IKZF1/3." Blood 128, no. 22 (2016): 4477. http://dx.doi.org/10.1182/blood.v128.22.4477.4477.

Full text

Abstract:

Abstract Introduction: Bay 61-3606 is a cell-permeable imidazopyrimidine compound that acts as a potent, ATP-competitive, reversible, and highly selective inhibitor of Syk tyrosine kinase activity with no inhibitory effect against Btk, Fyn, Itk, Lyn, and Src. BAY 61-3606 has been also shown to inhibit Syk-mediated cellular functions such as glucose-tyrosine phosphorylation of I κ B α and p65 nuclear translocation. It further exhibits a good oral bioavailability and in vivo efficacy in rat models. Recently, Bay 61-3606 was found to inhibit cell proliferation and SDF-1a-induced migration of MM c

APA, Harvard, Vancouver, ISO, and other styles

44

Mullard, Asher. "FDA approves first-in-class SYK inhibitor." Nature Reviews Drug Discovery 17, no. 6 (2018): 385. http://dx.doi.org/10.1038/nrd.2018.96.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Zhang, Pengyu, Fiorella A. Solari, Johan W. M. Heemskerk, et al. "Differential Regulation of GPVI-Induced Btk and Syk Activation by PKC, PKA and PP2A in Human Platelets." International Journal of Molecular Sciences 24, no. 9 (2023): 7776. http://dx.doi.org/10.3390/ijms24097776.

Full text

Abstract:

Bruton’s tyrosine kinase (Btk) and spleen tyrosine kinase (Syk) are major signaling proteins in human platelets that are implicated in atherothrombosis and thrombo-inflammation, but the mechanisms controlling their activities are not well understood. Previously, we showed that Syk becomes phosphorylated at S297 in glycoprotein VI (GPVI)-stimulated human platelets, which limits Syk activation. Here, we tested the hypothesis that protein kinases C (PKC) and A (PKA) and protein phosphatase 2A (PP2A) jointly regulate GPVI-induced Btk activation in platelets. The GPVI agonist convulxin caused rapid

APA, Harvard, Vancouver, ISO, and other styles

46

Cremer, Anjali, Jana M. Ellegast, Yana Pikman, et al. "Resistance Mechanisms to SYK Inhibition in AML." Blood 132, Supplement 1 (2018): 2638. http://dx.doi.org/10.1182/blood-2018-99-114996.

Full text

Abstract:

Abstract Alterations in signaling pathways are critical to the pathogenesis of acute myeloid leukemia (AML) and are often driven by aberrant kinases. We previously identified spleen tyrosine kinase (SYK), a non-receptor, cytoplasmic tyrosine kinase, as a druggable target in AML and a critical regulator of FLT3, the most commonly mutated receptor tyrosine kinase in this disease. SYK was initially described as having an important role in B-cell development. More recent studies showed a broader relevance of SYK in hematopoietic signaling. Multiple orally bioavailable SYK inhibitors, including ent

APA, Harvard, Vancouver, ISO, and other styles

47

Aguirre-Ducler, Adam, Nicole Gianino, Franz Villarroel-Espindola та ін. "Tumor cell SYK expression modulates the tumor immune microenvironment composition in human cancer via TNF-α dependent signaling". Journal for ImmunoTherapy of Cancer 10, № 7 (2022): e005113. http://dx.doi.org/10.1136/jitc-2022-005113.

Full text

Abstract:

BackgroundThe expression of SYK in cancer cells has been associated with both tumor promoting and tumor suppressive effects. Despite being proposed as anticancer therapeutic target, the possible role of SYK in modulating local adaptive antitumor immune responses remains uncertain. Using detailed analysis of primary human tumors and in vitro models, we reveal the immunomodulatory effect of SYK protein in human solid cancer.MethodsWe spatially mapped SYK kinase in tumor cells, stromal cells and tumor-infiltrating leukocytes (TILs) in 808 primary non-small cell lung carcinomas (NSCLCs) from two c

APA, Harvard, Vancouver, ISO, and other styles

48

Burke, Russell T., Astrid Clarke, Sarah A. Meadows та ін. "A Potential Therapeutic Strategy for Chronic Lymphocytic Leukemia by Combining GS-1101, a PI3 kinase Delta (PI3Kδ) Inhibitor and a Novel Highly Selective Spleen Tyrosine Kinase (Syk) Inhibitor, GS-9973". Blood 120, № 21 (2012): 3876. http://dx.doi.org/10.1182/blood.v120.21.3876.3876.

Full text

Abstract:

Abstract Abstract 3876 Background: Chronic lymphocytic leukemia (CLL) is the most common leukemia in the Western World and remains incurable with standard therapies. Despite significant advances, novel treatments are essential to improve outcomes. A number of therapeutic agents have recently been developed including some that have shown significant activity and tolerability in clinical trials. Among these drugs, are small molecule kinase inhibitors that inhibit B-cell receptor (BCR)-mediated signaling pathways and disrupt essential CLL cell-microenvironment interactions. Specifically, when pri

APA, Harvard, Vancouver, ISO, and other styles

49

Witzig, Thomas E., and Mamta Gupta. "Signal Transduction Inhibitor Therapy for Lymphoma." Hematology 2010, no. 1 (2010): 265–70. http://dx.doi.org/10.1182/asheducation-2010.1.265.

Full text

Abstract:

Abstract Current research in lymphoma is focused on two areas of lymphoma biology—the signal transduction pathways used to maintain the growth of malignant lymphocytes and the role of the tumor microenvironment in lymphoma growth and survival. This review focuses on three signaling pathways: the phosphatidylinositol 3-kinase/mammalian target of rapamycin (PI3K/mTOR) pathway, the B-cell receptor/spleen tyrosine kinase (BCR/Syk) pathway, and the protein kinase C-beta (PKC-β) pathway, known to be important to lymphoma cells. The mTOR inhibitors temsirolimus and everolimus have demonstrated antitu

APA, Harvard, Vancouver, ISO, and other styles

50

Hatton, Olivia, Stacie Lambert, Sheri Krams, and Olivia Martinez. "Syk survival signals in Epstein-Barr virus + B cell lymphomas (165.27)." Journal of Immunology 186, no. 1_Supplement (2011): 165.27. http://dx.doi.org/10.4049/jimmunol.186.supp.165.27.

Full text

Abstract:

Abstract EBV latent membrane protein 2a (LMP2a) is a B cell receptor mimic that provides a constitutive survival signal to virally-infected cells through Syk; however, the precise downstream mechanisms executing this survival signal have yet to be elucidated. Previously, we have shown that Syk inhibition induces apoptosis and reduces PI3K/Akt and Erk downstream signals in our EBV+ B cell lymphoma lines. Small molecule inhibitors for the Syk, PI3K/Akt and Erk pathway, or a DMSO vehicle control, were used to interrogate the function of each pathway. Survival of EBV+ B cell lymphoma lines was dep

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!