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Literatura académica sobre el tema "Syk Inhibitor"

Autor: Grafiati
Publicado: 11 de marzo de 2023

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Artículos de revistas sobre el tema "Syk Inhibitor"

1

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.

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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 and tissues. Methods: Cell proliferation was measured with WST-1 reagent. Apoptotic assay was performed with Annexin-V and 7-AAD by flow cytometry (FC, FACSCalibur, BD Bioscience). Phospho-Src (Y416) antibody (cell signaling Technology, CSL) was used for immunoblotting and immunohistochemistry. (IHC, Discovery, Ventana Medical Systems). Phospho-Syk (Y525/526) antibody (CSL) was used for FC and immunoblotting. Results: In a screening for the effects of different kinases’ inhibitors on B-cell lymphoma lines, we observed that SFK inhibitors, PP2 and dasatinib (Sprycel, Bristol Myers Squibb), inhibited proliferation and caused dose-dependent apoptosis induction at 24 h (PP2: 31% at 10 mM; dasatinib: 39% at 100 nM) in Burkitt’s lymphoma cell line Raji. The apoptotic induction was associated with cleavage of caspase-3 and caspase-8. The ability of SFK inhibitors to induce apoptosis in Raji cells paralleled high level expression of constitutive phospho- SFK (Y416). In contrast to this Burkitt’s line, diffuse large B-cell lymphoma (DLBCL) lines (Sud-HL4, Sud-HL-6 and OCI-LY3, OCI-LY10) were less-sensitive to these SFK inhibitors but showed apoptosis induction upon exposure to the Syk inhibitor (piceatannol & syk inhibitor IV). Interestingly, the DLBCL lines that were resistant to SFK inhibitors had undectable or low levels of phospho-SFK (Y416); while their susceptibility to the Syk inhibitor-induced apoptosis paralleled detectable constitutive phospho-Syk (Y525/526). Immunohistochemical staining of burkitt’s lymphoma tissues and a tissue microarray panel of NHL indicated 13/20 (65%) of Burkitt’s lymphoma, 3/5 of small lymphocytic lymphoma, 2/5 of mantle cell lymphoma, 3/10 of follicular lymphoma, 2/5 of DLBCL, 2/5 of marginal zone lymphoma, 1/5 of lymphoblastic lymphoma are positive for phospho-Src (Y416). Staining of normal tonsil tissue showed germinal center cells are strong positive for phospho-Src (Y416), while marginal zone cells are weak positive and plasma cells are negative. We are currently testing the correlation of phospho-Src (Y416) expression in fresh NHL tissues and their sensitivity to Src family kinase inhibitors. Conclusion: These data suggest that rational application of molecularly targeted therapy for aggressive NHL is possible by directly examining key signaling nodes promoting survival and proliferation. For instance, the clinical SFK inhibitor dasatinib is currently being examined in a clinical trial for NHL (NCT00550615). Our results suggest that profiling patients’ lymphoma cells for phospho-SFK could optimize therapeutic efficacy and minimize unnecessary treatment-related side effects.
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2

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.

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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, the GPVI-agonist convulxin, and the GPIbα-agonist echicetin beads (EB) were used to stimulate human platelets with/without effectors. Platelet aggregation and intracellular messengers were analyzed, along with phosphoproteins, by immunoblotting using phosphosite-specific antibodies or phos-tags. ADP, convulxin, and EB upregulated Syk S297 phosphorylation, which was inhibited by iloprost (cAMP pathway). Convulxin-stimulated Syk S297 phosphorylation was stoichiometric, transient, abolished by the PKC inhibitor GF109203X, and mimicked by the PKC activator PDBu. Convulxin/EB stimulated Syk S297, Y352, and Y525/526 phosphorylation, which was inhibited by SFK and Syk inhibitors. GFX and iloprost inhibited convulxin/EB-induced Syk S297 phosphorylation but enhanced Syk tyrosine (Y352/Y525/526) and substrate (linker adaptor for T cells (LAT), phospholipase γ2 (PLC γ2)) phosphorylation. GFX enhanced convulxin/EB-increases of inositol monophosphate/Ca2+. ITAM-activated Syk stimulates PKC-dependent Syk S297 phosphorylation, which is reduced by SFK/Syk/PKC inhibition and cAMP. Inhibition of Syk S297 phosphorylation coincides with enhanced Syk activation, suggesting that S297 phosphorylation represents a mechanism for feedback inhibition in human platelets.
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3

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.

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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 of the proinflammatory cytokine/chemokine, IL-6 and CXCL8 from BEAS-2B and CFBE41o- epithelial cells by Pa. Effects of a Syk inhibitor against phosphorylation of the MAPKs were also evaluated. IL-6 and CXCL8 release by Pa were significantly inhibited by p38MAPK and Syk inhibitors (p<0.05). Phosphorylation of HSP27, but not ERK or JNK, was significantly inhibited by Syk kinase inhibition. A combination of p38MAPK and Syk inhibitors showed synergy against IL-6 and CXCL8 induction and an NSKI completely inhibited IL-6 and CXCL8 at low concentrations. Pa-induced inflammation is dependent on p38MAPK primarily, and Syk partially, which is upstream of p38MAPK. The NSKI suggests that inhibiting specific combinations of kinases is a potent potential therapy for Pa-induced inflammation.
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4

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.

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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 degranulation activity of the active compounds. Finally, tanshinone I was confirmed as a Syk inhibitor (IC50 = 1.64 μM) and exhibited anti-mast cell degranulation activity in vitro (IC50 = 2.76 μM). Docking studies showed that Pro455, Gln462, Leu377, and Lys458 were key amino acid residues for Syk inhibitory activity. This study demonstrated that tanshinone I is a Syk inhibitor with mast cell degranulation inhibitory activity. Tanshinone I may be a potential lead compound for developing effective and safe Syk-inhibiting drugs.
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5

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.

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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; Mahadevan et al, w Streubel et al, 2006), suggesting SYK targeting agents could be useful for the treatment of various lymphoma subtypes. SYK inhibitors are already in clinical development for treatment of asthma. Here, we report on the activity on lymphoma cell lines and primary cells of the SYK/ZAP-70 inhibitor #1 (Novartis) and of the BCR-ABL inhibitors imatinib (Novartis) and nilotinib (Novartis), which could act as cross-selecting SYK inhibitors (Atwell et al, 2004). We treated four human MCL and three DLBCL established cell lines with increasing doses of the SYK/ZAP-70 inhibitor #1, imatinib and nilotinib for 72 h. Cell viability was measured with the MTT assay. The two cell lines expressing high levels of SYK, JeKo-1 and SUD-HL-6, were sensitive to the compounds (IC50: Syk/ZAP-70 inhibitor #1, 1–5 μM; imatinib, 15–20 μM; nilotinib, 10 μM). Cells with lower SYK expression were generally less sensitive to all three compounds. To obtain further data on the relevance of SYK inhibition in lymphoma, we treated nine lymphoma primary cells with the piceatannol (Sigma), the SYK/ZAP-70 inhibitor #1 and nilotinib. Responses, defined as <50% decrease in viable cell number, were observed with piceatannol (4/9 samples), the Syk/ZAP-70 inhibitor #1 (3/9 samples) and nilotinib (3/9 samples). Immunoblotting experiments aimed to elucidate the mechanism of action are under-way and data will be presented at the meeting. In conclusion, our data indicate that pharmacological inhibition of SYK is a therapeutic approach to be further investigated in subsets of aggressive lymphomas.
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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.

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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 profiling identified enhanced expression of SYK and downstream pathways in CLL compared to healthy B cells. Immunoblotting showed increased expression and phosphorylation of SYK, PLCγ2, STAT3, and ERK1/2 in CLL compared to healthy B cells suggesting enhanced activation of these mediators in CLL. Separate analyses according to prognostic parameters revealed 1.8-fold higher SYK protein level in unmutated compared to mutated CLL cells determined by densitometric analysis (n=22, p=0.0031). These findings may well explain the higher BCR signaling capacity in the unmutated CLL subset. Various SYK inhibitors (piceatannol, curcumin, SYK Inhibitor II, and IV (Calbiochem)) reduced phosphorylation of the SYK downstream targets PLCγ2, STAT3, and ERK1/2 in a time- and dose-dependent manner and induced apoptosis in the CLL cell lines Mec-1 and EHEB and primary CLL cells. SYK Inhibitor II revealed highest cytotoxic effects on primary CLL cells, but did not significantly reduce the viability of healthy B cells. Thus, apoptotic effects of this inhibitor were analyzed in a larger cohort of patient samples along with the well-established SYK inhibitor R406 (Rigel Inc.). After 48 hour treatment, relative viability of CLL cells was reduced to 76% and 44% for SYK Inhibitor II (4 mM and 10 mM) and to 66% for R406 (4 mM), respectively (n=38, p<0.0001). With respect to prognostic factors, SYK inhibitors exerted stronger cytotoxic effects in unmutated and ZAP70+ cases. Cytotoxicity of SYK inhibitors were associated with SYK protein expression potentially predicting response to therapy (Pearson correlation coefficient: r=0.78 for SYK Inhibitor II (p<0.0001) and r=0.56 for R406 (p=0.0134)). Combination of fludarabine with SYK Inhibitor II or R406 increased cytotoxicity compared to fludarabine therapy alone. The mean viability of F-ara-A treated cells (10 mM) was reduced by 13% with SYK II and by 17% with R406 (n=10, p<0.0001), respectively. Since microenvironment enhances the viability of CLL cells and decreases their sensitivity towards chemotherapy, apoptosis rates of CLL cells incubated with SYK Inhibitor II in the presence and absence of the stromal cell line M2-10B4 were assayed. No significant change in cytotoxic effects was observed. Hence, stromal cell interactions do not impair the cytotoxicity of SYK inhibitors. Moreover, CD40L expressing T cells play an important role in the CLL microenvironment, and CD40 ligation is under discussion to induce fludarabine resistance in CLL. Therefore the effect of SYK Inhibitor II in combination with CD40 ligation was analyzed. In contrast to conventional chemotherapy, stimulation with CD40L significantly sensitized CLL cells towards SYK inhibition. In conclusion, this work establishes SYK inhibition as a rational and promising therapeutic principle in CLL. Given the preferential activity of SYK inhibitors in CLL cases with poor prognostic factors, the independence of their activity from the protective influence of the CLL microenvironment, and the synergistic and complementary action with fludarabine, we propose SYK inhibitors for clinical assessment in the therapy of CLL.
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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.

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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 PI3Kδ were approved recently by FDA for treatment of some subtypes of B-cell malignancies. Currently, a couple small molecular inhibitors against SYK, another BCR downstream molecule, are under the early clinical development and showed initial efficacy in B cell lymphomas. HMPL-523, discovered and currently being developed in Phase I clinical trial by Hutchison MediPharma, is a novel, highly potent and selective SYK inhibitor (IC50: 0.025 μM). The anti-tumor activity of HMPL-523 was evaluated in this study. Methods: Inhibitory effects of HMPL-523 on cell viability were investigated in a panel of B cell lymphoma cell lines with SYK/BCR dysregulation by CellTiter-Glo luminescent or CCK-8 assay. The effect of HMPL-523 on SYK signaling pathway was detected by western blot. Annexin-V- positive and PI-negative population was recognized as apoptotic cells by FACS. Nude mice bearing B cell lymphoma xenograft tumors with SYK/BCR dysregulation were used to determine anti-tumor activity of HMPL-523 in vivo. Result: HMPL-523 blocked phosphorylation of BLNK, downstream protein of Syk, in human mantle cell line REC-1 and human plasma cell line ARH-7777 with IC50 of 0.105 µM and 0.173 μM, respectively. HMPL-523 also inhibited cell viability of Ba/F3 Tel-Syk with IC50 of 0.033 μM. Furthermore, inhibitory effects of HMPL-523 on cell viability were evaluated in a panel of B -cell lymphoma cell lines with SYK/BCR deregulation. Results showed that HMPL- 523 potently inhibited cell survival with IC50s from 0.4 to 2 μM. Consistent with the effect on cell viability, HMPL-523 increased the apoptotic rate of REC-1 cells. Moreover, HMPL-523 showed the synergistic activities on killing human diffused large B cell lymphoma (DLBCL) in combination with other drugs such as BTK inhibitor, PI3Kδ inhibitors and Bcl2 family inhibitor. The detailed mechanisms underlying the synergism are still under investigation. Anti-tumor activity of HMPL-523 was determined in Syk dependent xenograft models. Daily oral administration of 100 mg/kg HMPL-523 showed potent anti-tumor activity in B cell lymphoma REC-1 (TGI: 59%). Conclusion:HMPL-523 is a highly potent SYK inhibitor with good activity against B-cell lymphoma in pre-clinical in vitro and in vivo models, supporting further clinical research for HMPL-523 as either single agent or combination drug with other agents to treat B-cell malignancies e.g. DLBCL Disclosures Yang: Hutchison MediPharma Ltd: Employment, Research Funding. Deng:Hutchison MediPharma Ltd: Employment, Research Funding. Sun:Hutchison MediPharma Ltd: Employment, Research Funding. Liang:Hutchison MediPharma Ltd: Employment, Research Funding. Wang:Hutchison MediPharma Ltd: Employment, Research Funding. Fan:Hutchison MediPharma Ltd: Employment, Research Funding. Tang:Hutchison MediPharma Ltd: Employment, Research Funding. Yu:Hutchison MediPharma Ltd: Employment, Research Funding. Sun:Hutchison MediPharma Ltd: Employment, Equity Ownership. Zhou:Hutchison MediPharma Ltd: Employment, Research Funding. Dai:Hutchison MediPharma Ltd: Employment, Research Funding. Qing:Hutchison MediPharma Ltd: Employment, Research Funding. Su:Hutchison MediPharma Ltd: Employment, Research Funding. Ren:Hutchison MediPharma Ltd: Employment, Research Funding.
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8

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.

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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 that pharmacological inhibition of Syk could attenuate the EGF-induced phosphorylation of EGFR, JNK, p38 MAPK, STAT1, and STAT3 in A431, CAL27 and SAS cells. In addition, EGF could induce a Syk-dependent IL-8 gene and protein expression in SCC. Confocal microscopic data demonstrated the ability of the Syk inhibitor to change the subcellular distribution patterns of EGFR after EGF treatment in A431 and SAS cells. Moreover, according to Kaplan-Meier survival curve analysis, higher Syk expression is correlated with poorer patient survival rate and prognosis. Notably, both Syk and EGFR inhibitors could induce PARP activation, and synergistic cytotoxic actions were observed in SCC cells upon the combined treatment of the PARP1 inhibitor olaparib with Syk or the EGFR inhibitor. Collectively, we reported Syk as an important signalling molecule downstream of EGFR that plays crucial roles in SCC development. Combining Syk and PARP inhibition may represent an alternative therapeutic strategy for treating SCC.
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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.

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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-induced platelet aggregation was unaffected in FcRγ-chain null murine platelets, ruling out the possibility of glycoprotein VI-mediated events. More interesting, OXSI-2 and Go6976, two structurally unrelated inhibitors shown to affect Syk, had only a partial effect on DxS-induced PAC-1 binding. DxS-induced platelet aggregation and intracellular calcium increases were abolished by the pan PI-3 kinase inhibitor LY294002, or an isoform-specific PI-3 kinase β inhibitor TGX-221. Pretreatment of platelets with Syk inhibitors or ADP receptor antagonists had little effect on Akt phosphorylation following DxS stimulation. These results, for the first time, establish a novel tyrosine kinase pathway in platelets that causes fibrinogen receptor activation in a PI-3 kinase-dependent manner without a crucial role for Syk.
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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.

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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) demonstrated spontaneous elevation of LPS and BG in serum from gut translocation despite the similarity in faecal microbiome analysis. Syk abundance in FcgRIIb–/– mice was higher than in pristane mice, possibly due to several Syk activators (anti-dsDNA, LPS and BG), and Syk inhibitor–attenuated proteinuria and serum cytokines only in FcgRIIb–/– mice. In addition, LPS + BG enhanced the expression of activating FcgRs, NF-κB and Syk, together with supernatant TNF-α predominantly in FcgRIIb–/– compared to wild-type macrophages. The inhibitors against Dectin-1, Syk and nuclear factor kappa B, but not anti-Raf-1, reduced supernatant TNF-α in LPS+BG-activated macrophages, implying Syk-dependent signalling. The pathogen molecules enhanced activating-FcgRs, without inhibition, through Syk, a shared downstream innate and adaptive signalling, is responsible for the hyper-responsiveness in FcgRIIb–/– macrophages. In conclusion, Syk inhibitor attenuated inflammation in FcgRIIb–/– but not in pristane mice, implying the influence of a lupus genetic background in treatment modalities.
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Tesis sobre el tema "Syk Inhibitor"

1

Yamamoto, Noriyuki. "Development of a selective inhibitor for Syk tyrosine kinase and investigation of its pharmacological activities." 京都大学 (Kyoto University), 2003. http://hdl.handle.net/2433/148369.

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Roders, Nathalie. "Régulation de l'activation de lymphocytes B / cellules plasmatiques pendant le rejet chronique : Le rôle de SYK dans la modulation de Mcl-1." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS439/document.

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L'insuffisance rénale est un problème majeur de santé publique et la transplantation rénale est l’option thérapeutique principale, mais elle comporte le risque de rejet d'organe. Les cellules B jouent un rôle important dans le rejet médié par les anticorps (AMR). Au cours de l'AMR chronique, les structures lymphoïdes tertiaires, semblables aux centres germinatifs (GC), apparaissent dans l'organe rejeté, associées à la production des plasmocytes et des lymphocytes B mémoires spécifiques du donneur. Ces populations de lymphocyte B sont souvent mal contrôlées par les traitements actuels. La myeloid cell leukemia 1 (Mcl-1), un membre anti-apoptotique de la famille de B-cell lymphoma 2 (Bcl-2), est essentiel pour maintenir l’organisation de GC et de la différenciation des cellules B. Nous rapportons ici l'infiltration de cellules B exprimant Mcl-1 dans le rein de patients atteints d'AMR chronique, comme cela a été observé pour les cellules (pré) GC. Suite à l’abrogation de la signalisation du récepteur des cellules B (BCR), par l'inhibition de la spleen tyrosine kinase (SYK) nous avons observé une diminution de la viabilité des cellules GC, par l'intermédiaire d'une régulation de Mcl-1. La régulation négative de Mcl-1 est coordonnée au niveau de la transcription, potentiellement par l'intermédiaire du transducteur de signal et de l'activateur de la transcription 3 (STAT3), comme cela a été observé par (1) une translocation altérée de STAT3 dans le noyau suivant l'inhibition de SYK, et (2) les niveaux inférieurs de transcription de Mcl-1. Par ailleurs, la surexpression de Mcl-1 inhibe l'apoptose après l'inhibition du SYK. Des études avec des cellules B primaires, issues d'amygdales, ont confirmé que l'inhibition de SYK a diminué la survie cellulaire. Nous avons également constaté que l'inhibition du SYK a diminué les niveaux de protéines Mcl-1 dans les cellules B primaire, et que l’activation de ces cellules a été inhibée, tel que déterminé par l'expression de CD80 et des taux inférieurs de sécrétion d'IgG dans les cellules B primaires activées in vitro. Nos travaux suggèrent que la voie SYK-Mcl-1 peut offrir de nouvelles opportunités pour le traitement et la prévention de l'AMR<br>Renal failure is a major public health concern and renal transplantation is the main therapeutic option, however it comes with the risk of organ rejection. B-cells play an important role in antibody-mediated rejection (AMR). During chronic AMR, tertiary lymphoid germinal center (GC)-like structures appear in the rejected organ, associated with de novo production of donor-specific plasma and memory B-cells. Which are B-cell populations that are often poorly controlled by current treatments. Myeloid cell leukemia-1 (Mcl-1), an anti-apoptotic member of the B-cell lymphoma-2 (Bcl-2) family, is essential for maintaining the GC reaction and B-cell differentiation. We report here the infiltration of B-cells expressing Mcl-1 in the kidney of patients with chronic AMR, as observed for (pre-)GC cells. The impairment of B-cell receptor (BCR) signaling, by inhibition of spleen tyrosine kinase (SYK), reduced viability and Mcl-1 protein levels in GC like cells. This downregulation is coordinated at the transcriptional level, potentially via signal transducer and activator of transcription 3 (STAT3), as shown by (1) impaired translocation of STAT3 to the nucleus following SYK inhibition, and (2) the lower levels of Mcl-1 transcription upon STAT3 inhibition. Moreover, overexpression of Mcl-1 prevented cells from entering apoptosis after SYK inhibition. In vitro studies with primary tonsillar B-cells confirmed that SYK inhibition decreased cell survival. We also found that SYK inhibition decreased Mcl-1 protein levels in primary B-cells, and that B-cell activation was inhibited, as determined by CD80 expression and lower levels of IgG secretion in tonsillar B-cells activated in vitro. Overall, our data suggest that the SYK-Mcl-1 pathway may provide new opportunities for the treatment and prevention of AMR
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Abadleh, Mohammed Mustafa Mohammed. "Diarylisoxazole als Leitstruktur für Design und Synthese von Proteinkinase Inhibitoren = Diarylisoxazoles as lead for the design and synthesis of protein kinase inhibitors /." Tübingen, 2009. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000276718.

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Xu, Mingming. "Discovery of inhibitors against a-synuclein aggregation." Thesis, Griffith University, 2020. http://hdl.handle.net/10072/392373.

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Abnormal protein aggregation has been linked to many neurodegenerative diseases, including Parkinson’s disease (PD). The main pathological hallmark of PD is the formation of Lewy bodies and Lewy neurites, both containing the pre-synaptic protein α-synuclein (α-syn). Native α-syn, under normal conditions, exists in a soluble unfolded state but undergoes misfolding and aggregation into toxic aggregates under pathological conditions. Toxic α-syn species can cause oxidative stress, membrane penetration, synaptic and mitochondrial dysfunction, leading to neuronal death and eventually neurodegeneration. Currently, early diagnosis and treatments targeting PD pathogenesis are urgently needed. Given its critical role in PD, α-syn is an attractive target for the development of both diagnostic tools and effective therapeutics. This thesis consists of a series of published and unpublished papers. In Chapter 1, which was published as a review, the progress towards discovering imaging probes and aggregation inhibitors for α-syn was summarized. Since a key property of such required therapeutic agents is specific binding to the target protein, relevant strategies and techniques in the discovery of α-syn-targeted drugs are discussed. As my PhD project aimed to screen small molecules capable of binding to α-syn specifically and then discover new α-syn aggregation inhibitors from the screened structures, relevant techniques were discussed at the end of Chapter 1. Mass spectrometry was chosen to discover specific α-syn binding molecules as this technique allows rapid detection of direct interactions between molecules and proteins. The materials and methods that were used in the included publications, were summarized in detail in Chapter 2. To provide sufficient protein for our study, the in-house α-syn having equally good quality as the commercial protein, was successfully generated in Chapter 3. Also, high yield of pure protein can be acquired from medium scale of bacteria culture, saving plenty of time and money for preparing proteins for large-scale screening. The protein expression and purification was a part of the supplementary data in the publication included in Chapter 4, where an automated screening system based on the connection of a mass spectrometer and the auto-sampler from a high performance liquid chromatograph was successfully established. This system allows computer-controlled sample loading and data acquisition with high stability and reproducibility. We first discovered a new inhibitor by screening over 4,300 pure molecules. The new compound, 3-[(3-methoxyphenyl)carbamoyl]-7-[(E)-2-phenylethenyl]-4,7- dihydropyrazolo [1,5-a]pyrimidine-5-carboxylic acid, not only significantly inhibited the misfolding and aggregation of α-syn, protected neuroblastoma cells from α-syn toxicity, but also has a more specific binding site compared with positive controls. The capability of the MS-based screening was further extended to the discovery of active components from natural products (manuscript in submission). A total of 29 marine fractions from our collaborators, were tested by MS and a new cholesterol derivative with significant inhibition of α-syn aggregation, was discovered and isolated from the active fraction. This MS-guided isolation of active components from natural products can also be applied to investigating traditional Chinese medicines with known therapeutic effects. Post-translational modifications (PTMs) of α-syn, especially enzymatic glycosylation with N-acetylglucosamine (GlcNAc) onto the proteins hydroxylated amino acid residues, have been reported to affect the pathogenic self-assembly of α-syn. As such, manipulation of the proteins’ O-GlcNAcylation statuses has been proposed to offer a therapeutic route toward addressing PD. In Chapter 5, small peptides with different sequences and modification sites were synthesized by our collaborators. In the thioflavin-T assay, which is a golden standard for measuring α-syn aggregation, two peptides with O-GlcNAcylation at the serine site exhibited significant inhibition. Therefore, small glycopeptides that couple the protective effects of O-GlcNAc with the selectivity of recognition sequences may prove useful tools to modulate α-syn aggregation (manuscript under review). Other sources of compounds including new analogs of anle138b, which is a well-studied α-syn aggregation modulator, were evaluated. Two derivatives of anle138b exerted promising effects on the aggregation of α-syn. Interestingly, these synthesized compounds and peptides did not form protein-ligand complexes in the mass spectra, indicating that these molecules, unlike the compounds we discovered in Chapter 4, may interact with α-syn aggregates instead of α-syn monomers. In the last chapter, general conclusions of the thesis were made and future directions were also discussed.<br>Thesis (PhD Doctorate)<br>Doctor of Philosophy (PhD)<br>School of Environment and Sc<br>Science, Environment, Engineering and Technology<br>Full Text
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Coombes, Susan. "Boards of directors and nonprofit entrepreneurial orientation Catalyst, inhibitor, or inconsequential /." Related electronic resource: Current Research at SU : database of SU dissertations, recent titles available full text, 2008. http://wwwlib.umi.com/cr/syr/main.

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Bracht, Kathrin. "Neue Inhibitoren zellmembranständiger Proteinkinasen /." Konstanz, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000252796.

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Cohen, Jason C. "Attention mechanisms and inhibition of return in the somatosensory system." Related electronic resource: Current Research at SU : database of SU dissertations, recent titles available full text, 2002. http://wwwlib.umi.com/cr/syr/main.

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Amanovic, Ilijana. "Ginkgo biloba extract inhibits tissue factor degradation /." [S.l.] : [s.n.], 2009. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000278514.

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Wollmann, Heike. "MiRNA targeting mechanisms - translation inhibition versus transcript cleavage /." Tübingen, 2009. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000251923.

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Bühler, Nico Martin. "Selektive COX-2 Inhibitoren und Nierenschädigung bei salzsensitiver Hypertonie /." [S.l.] : [s.n.], 2009. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000297941.

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Libros sobre el tema "Syk Inhibitor"

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Remer, Imke Ilina. Syk-Inhibition mit Fostamatinib reduziert die Makrophagenakkumulation in atherosklerotischen Plaques. s.n.], 2014.

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Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.
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Capítulos de libros sobre el tema "Syk Inhibitor"

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Ishida, Yoji. "Others (Syk Inhibitor and Other Medications)." In Autoimmune Thrombocytopenia. Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4142-6_18.

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Denyer, Jane, and Vipul Patel. "Syk kinase inhibitors." In New Drugs and Targets for Asthma and COPD. KARGER, 2010. http://dx.doi.org/10.1159/000320832.

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Fleischmann, Roy. "Signalling pathway inhibitors." In Oxford Textbook of Rheumatology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081_update_003.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and other pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Many of the pro-inflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Spleen tyrosine kinase (SyK) is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling should interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib, approved in many countries for the treatment of RA, is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2; there are other JAK inhibitors in development which are purported to be more specific for JAK3 (Vertex 509), specific for JAK1/2 (baricitinib) or more specific for JAK1 (Galapagos and INCYTE) where clinical data has been reported. Tofacitinib has been investigated in multiple clinical trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎‎) and in patients who have failed TNFα‎‎ inhibitors. Vertex 509 has been investigated as monotherapy or in combination with MTX in DMARD failures while baricitinib, GLPG0634 (Galapagos), and INCB039110 (Incyte) have been investigated in phase 1 and 2 clinical trials in combination with MTX. Each of these medications has demonstrated efficacy; their safety profile has been shown to be generally similar although with some differences from each other and some differences from most of the currently approved biological agents. Fostamatinib disodium is an orally available inhibitor of SyK which was investigated in multiple phase 3 clinical trials in RA but was found to be generally ineffective with significant safety signals. This chapter discusses what is currently known and understood about the efficacy and safety of these oral, small-molecule DMARDs.
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Singh, Rajinder, and Esteban S. Masuda. "Chapter 24 Spleen Tyrosine Kinase (Syk) Biology, Inhibitors and Therapeutic Applications." In Annual Reports in Medicinal Chemistry Volume 42. Elsevier, 2007. http://dx.doi.org/10.1016/s0065-7743(07)42024-3.

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Kumar Chatterjee, Swapan, Snigdha Saha, and Shahin Muhammed T.K. "COVID-19 and Its Impact on Onset and Progression of Parkinson’s and Cognitive Dysfunction." In COVID-19 Pandemic, Mental Health and Neuroscience - New Scenarios for Understanding and Treatment [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.105667.

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In the COVID-19 pandemic, neurological complications have emerged as a significant cause of morbidity and mortality. A wide range of neurological manifestations ranging from cognitive or memory disturbances, headache, loss of smell or taste, confusion, and disabling strokes have been reported during and post COVID conditions. The COVID-19 virus can utilize two possible pathways for invasion into the brain, either through retrograde axonal transport (olfactory route) or by crossing the blood-brain barrier (BBB). Furthermore, the production of SARS-CoV-2-associated cytokines, such as interleukin (IL)-6, IL-17, IL-1b, and tumor necrosis factor (TNF), is able to disrupt the BBB. The neuroinvasive nature of SARS-CoV-2 has a more severe impact on patients with preexisting neurological manifestations such as Parkinson’s disease (PD). Pathological features of PD include selective loss of dopaminergic neurons in the substantia nigra pars compacta and aggregation of α-syn proteins present in neurons. Interaction between SARS-COV-2 infection and α-synuclein might have long-term implications on the onset of Parkinsonism by the formation of toxic protein clumps called amyloid fibrils—a hallmark of Parkinson’s. Molecular modeling is an emerging tool to predict potential inhibitors against the enzyme α-synuclein in neurodegenerative diseases by using plant bioactive molecules.
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Actas de conferencias sobre el tema "Syk Inhibitor"

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Lamb, David, Katherina Sewald, Ewald Benediktus, and Armin Braun. "Evaluating a CD63 assay as a biomarker for SYK inhibitor activity." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3301.

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Reddy, Sanjeeva, Nitin K. Damle, Aranapakam M. Venkatesan, et al. "Abstract 792: ASN002: A novel dual SYK/JAK inhibitor with strong antitumor activity." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-792.

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Chow, Chung-Wai, Patricia Castellanos Penton, Michelle North, Hajera Amatullah, Xiaomin Wang, and Jeremy Scott. "Treatment With Syk Inhibitor Attenuates Airway Hyperresponsiveness In A Chronic Murine Model Of Asthma." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2846.

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Joshi, Shweta, Kevin Liu, Muamera Zulcic, et al. "Abstract 109: Myeloid Syk-PI3Kg-HIF axis inhibits anti-tumor adaptive immunity:In silicodesign of a “first in class” novel dual-Syk/PI3K inhibitor, SRX3207, to block the immunosuppressive tumor microenvironment." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-109.

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Joshi, Shweta, Kevin Liu, Muamera Zulcic, et al. "Abstract 109: Myeloid Syk-PI3Kg-HIF axis inhibits anti-tumor adaptive immunity:In silicodesign of a “first in class” novel dual-Syk/PI3K inhibitor, SRX3207, to block the immunosuppressive tumor microenvironment." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-109.

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Sappal, Jessica J., Matthew Theisen, Zhongmin Xiang, et al. "Abstract 3844: TAK-659, a SYK kinase inhibitor, demonstrates preclinical antitumor activity in solid tumor models." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3844.

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Kim, Seon Uk, Hyun Jung Yoo, Shin Eui Kang, et al. "AB0126 ANTI-INFLAMMATORY EFFECTS OF SPLEEN TYROSINE KINASE (SYK) INHIBITOR, PICEATANNOL, ON FIBROBLAST-LIKE SYNOVIOCYTE IN RHEUMATOID ARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.6696.

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Tannheimer, Stacey L., Adam Kashishian, Rick Sorensen, and Kathleen S. Keegan. "Abstract 2371: Entospletinib, a potent SYK inhibitor, blocks constitutive and FCgRI activated signaling in FLT3-ITD cell lines." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2371.

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Allan, Richard, Ieuan Jones, Michael Bartley, Darren Wilbraham, and Dave Singh. "A Randomised, Placebo Controlled Trial Of The Effect Of An Inhaled Syk Inhibitor On Allergen Induced Airways Responses In Mild Asthma." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2774.

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Reddy, Sanjeeva P., Niranjan Rao, David Zammit, Scott K. Thompson, Roger A. Smith, and Louis Denis. "Abstract 4204: ASN002: A novel dual SYK/JAK inhibitor with strong antitumor activity in both hematological and solid tumor xenograft models." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4204.

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