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Article ; Online: Myeloma CAR-T CRS Management With IL-1R Antagonist Anakinra.

Jatiani, Shashidhar S / Aleman, Adolfo / Madduri, Deepu / Chari, Ajai / Cho, Hearn Jay / Richard, Shambavi / Richter, Joshua / Brody, Joshua / Jagannath, Sundar / Parekh, Samir

Clinical lymphoma, myeloma & leukemia

2020 Volume 20, Issue 9, Page(s) 632–636.e1

MeSH term(s)	Aged ; Humans ; Interleukin 1 Receptor Antagonist Protein/metabolism ; Male ; Multiple Myeloma/genetics ; Multiple Myeloma/pathology ; Receptors, Chimeric Antigen/genetics
Chemical Substances	Interleukin 1 Receptor Antagonist Protein ; Receptors, Chimeric Antigen
Language	English
Publishing date	2020-05-11
Publishing country	United States
Document type	Case Reports ; Research Support, N.I.H., Extramural
ZDB-ID	2540992-X
ISSN	2152-2669 ; 2152-2650
ISSN (online)	2152-2669
ISSN	2152-2650
DOI	10.1016/j.clml.2020.04.020
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Article ; Online: SOX11 Inhibitors Are Cytotoxic in Mantle Cell Lymphoma.

Jatiani, Shashidhar S / Christie, Stephanie / Leshchenko, Violetta V / Jain, Rinku / Kapoor, Abhijeet / Bisignano, Paola / Lee, Clement / Kaniskan, H Ümit / Edwards, Donna / Meng, Fanye / Laganà, Alessandro / Youssef, Youssef / Wiestner, Adrian / Alinari, Lapo / Jin, Jian / Filizola, Marta / Aggarwal, Aneel K / Parekh, Samir

Clinical cancer research : an official journal of the American Association for Cancer Research

2021 Volume 27, Issue 16, Page(s) 4652–4663

Abstract: Purpose: Mantle cell lymphoma (MCL) is a fatal subtype of non-Hodgkin lymphoma. SOX11 transcription factor is overexpressed in the majority of nodal MCL. We have previously reported that B cell-specific overexpression of SOX11 promotes MCL pathogenesis ... ...

Abstract	Purpose: Mantle cell lymphoma (MCL) is a fatal subtype of non-Hodgkin lymphoma. SOX11 transcription factor is overexpressed in the majority of nodal MCL. We have previously reported that B cell-specific overexpression of SOX11 promotes MCL pathogenesis via critically increasing BCR signaling Experimental design: Using a combination of Results: We find mechanistic validation of on-target activity of these SOX11i in the inhibition of BCR signaling and the transcriptional modulation of SOX11 target genes, specifically, in SOX11-expressing MCL cells. One of the three SOX11i exhibits relatively superior Conclusions: Taken together, our results provide a foundation for therapeutically targeting SOX11 in MCL by a novel class of small molecules.
MeSH term(s)	Animals ; Humans ; Lymphoma, Mantle-Cell/drug therapy ; Mice ; SOXC Transcription Factors/antagonists & inhibitors ; Tumor Cells, Cultured
Chemical Substances	SOX11 protein, human ; SOXC Transcription Factors ; Sox11 protein, mouse
Language	English
Publishing date	2021-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-20-5039
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Article: Expression of the antiviral protein MxA in cells transiently perturbs endocytosis.

Jatiani, Shashidhar S / Mittal, Rohit

Biochemical and biophysical research communications

2004 Volume 323, Issue 2, Page(s) 541–546

Abstract: MxA is an interferon-induced antiviral protein. Viral replication relies on the trafficking machinery of the host cell. Overexpression of MxA was found to perturb trafficking of internalized transferrin resulting in its accumulation in cells. ... ...

Abstract	MxA is an interferon-induced antiviral protein. Viral replication relies on the trafficking machinery of the host cell. Overexpression of MxA was found to perturb trafficking of internalized transferrin resulting in its accumulation in cells. Interestingly, this perturbation of endocytic trafficking was transient--with a maximal effect being seen 5-6 h after transfection. By 12 h after transfection the perturbation of endocytosis was seen to have subsided although MxA protein levels remained elevated even 24 h after transfection. The accumulation of transferrin is due to a block in transferrin recycling. It is further shown that MxA can physically associate with the endocytic protein dynamin, possibly accounting for the observed effect of MxA expression on transferrin endocytosis. These results uncover a hitherto unknown aspect of MxA action on trafficking processes within cells.
MeSH term(s)	Animals ; Antiviral Agents/metabolism ; CHO Cells ; Cricetinae ; Cricetulus ; Endocytosis/physiology ; GTP-Binding Proteins/genetics ; GTP-Binding Proteins/metabolism ; Gene Expression Regulation/physiology ; Homeostasis/physiology ; Myxovirus Resistance Proteins ; Protein Transport/physiology ; Time Factors ; Tissue Distribution
Chemical Substances	Antiviral Agents ; Myxovirus Resistance Proteins ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2004-10-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2004.08.134
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Article ; Online: SOX11 augments BCR signaling to drive MCL-like tumor development.

Kuo, Pei-Yu / Jatiani, Shashidhar S / Rahman, Adeeb H / Edwards, Donna / Jiang, Zewei / Ahr, Katya / Perumal, Deepak / Leshchenko, Violetta V / Brody, Joshua / Shaknovich, Rita / Ye, B Hilda / Parekh, Samir

Blood

2018 Volume 131, Issue 20, Page(s) 2247–2255

Abstract: Mantle cell lymphoma (MCL) is characterized by increased B-cell receptor (BCR) signaling, and BTK inhibition is an effective therapeutic intervention in MCL patients. The mechanisms leading to increased BCR signaling in MCL are poorly understood, as ... ...

Abstract	Mantle cell lymphoma (MCL) is characterized by increased B-cell receptor (BCR) signaling, and BTK inhibition is an effective therapeutic intervention in MCL patients. The mechanisms leading to increased BCR signaling in MCL are poorly understood, as mutations in upstream regulators of BCR signaling such as CD79A, commonly observed in other lymphomas, are rare in MCL. The transcription factor SOX11 is overexpressed in the majority (78% to 93%) of MCL patients and is considered an MCL-specific oncogene. So far, attempts to understand SOX11 function in vivo have been hampered by the lack of appropriate animal models, because germline deletion of SOX11 is embryonically lethal. We have developed a transgenic mouse model (Eμ-SOX11-EGFP) in the C57BL/6 background expressing murine SOX11 and EGFP under the control of a B-cell-specific IgH-Eμ enhancer. The overexpression of SOX11 exclusively in B cells exhibits oligoclonal B-cell hyperplasia in the spleen, bone marrow, and peripheral blood, with an immunophenotype (CD5
MeSH term(s)	Animals ; B-Lymphocytes/metabolism ; B-Lymphocytes/pathology ; Biomarkers ; Cell Line, Tumor ; Clonal Evolution ; Gene Expression ; Gene Expression Regulation, Neoplastic ; High-Throughput Nucleotide Sequencing ; Humans ; Immunoglobulin Heavy Chains ; Lymphoma, Mantle-Cell/genetics ; Lymphoma, Mantle-Cell/metabolism ; Lymphoma, Mantle-Cell/pathology ; Mice ; Mice, Transgenic ; Phenotype ; Receptors, Antigen, B-Cell/metabolism ; SOXC Transcription Factors/genetics ; SOXC Transcription Factors/metabolism ; Signal Transduction ; Tumor Microenvironment
Chemical Substances	Biomarkers ; Immunoglobulin Heavy Chains ; Receptors, Antigen, B-Cell ; SOXC Transcription Factors
Language	English
Publishing date	2018-04-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2018-02-832535
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Article ; Online: Jak/STAT pathways in cytokine signaling and myeloproliferative disorders: approaches for targeted therapies.

Jatiani, Shashidhar S / Baker, Stacey J / Silverman, Lewis R / Reddy, E Premkumar

Genes & cancer

2011 Volume 1, Issue 10, Page(s) 979–993

Abstract: Hematopoiesis is the cumulative result of intricately regulated signaling pathways that are mediated by cytokines and their receptors. Studies conducted over the past 10 to 15 years have revealed that hematopoietic cytokine receptor signaling is largely ... ...

Abstract	Hematopoiesis is the cumulative result of intricately regulated signaling pathways that are mediated by cytokines and their receptors. Studies conducted over the past 10 to 15 years have revealed that hematopoietic cytokine receptor signaling is largely mediated by a family of tyrosine kinases termed Janus kinases (JAKs) and their downstream transcription factors, termed STATs (signal transducers and activators of transcription). Aberrations in these pathways, such as those caused by the recently identified JAK2(V617F) mutation and translocations of the JAK2 gene, are underlying causes of leukemias and other myeloproliferative disorders. This review discusses the role of JAK/STAT signaling in normal hematopoiesis as well as genetic abnormalities associated with myeloproliferative and myelodisplastic syndromes. This review also summarizes the status of several small molecule JAK2 inhibitors that are currently at various stages of clinical development. Several of these compounds appear to improve the quality of life of patients with myeloproliferative disorders by palliation of disease-related symptoms. However, to date, these agents do not seem to significantly affect bone marrow fibrosis, alter marrow histopathology, reverse cytopenias, reduce red cell transfusion requirements, or significantly reduce allele burden. These results suggest the possibility that additional mutational events might be associated with the development of these neoplasms, and indicate the need for combination therapies as the nature and significance of these additional molecular events is better understood.
Language	English
Publishing date	2011-03-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2538519-7
ISSN	1947-6027 ; 1947-6019
ISSN (online)	1947-6027
ISSN	1947-6019
DOI	10.1177/1947601910397187
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Article: Conformational analysis of the GTP-binding protein MxA using limited proteolysis.

Varne, Anjali / Muthukumaraswamy, Karthika / Jatiani, Shashidhar S / Mittal, Rohit

FEBS letters

2001 Volume 516, Issue 1-3, Page(s) 129–132

Abstract: Guanosine triphosphate (GTP)-binding proteins are known to function as molecular switches that cycle between GTP-bound and guanosine diphosphate (GDP)-bound states. Switching is achieved by the fact that G-proteins in the GTP-bound conformation can ... ...

Abstract	Guanosine triphosphate (GTP)-binding proteins are known to function as molecular switches that cycle between GTP-bound and guanosine diphosphate (GDP)-bound states. Switching is achieved by the fact that G-proteins in the GTP-bound conformation can interact with a certain set of effector molecules while they interact with a different set of partners in their GDP-bound conformation. The antiviral properties of the interferon-induced MxA protein are critically dependent on the ability of MxA to bind GTP. Using limited proteolysis we analyzed the conformations of the MxA protein under nucleotide-free, GDP-bound, and GTP-bound conditions. We find that whereas the conformations of nucleotide-free MxA and GDP-bound MxA are essentially similar, GTP-binding causes a dramatic change in the conformation of MxA.
MeSH term(s)	Animals ; Antiviral Agents/chemistry ; Antiviral Agents/metabolism ; Endopeptidase K ; GTP-Binding Proteins/chemistry ; GTP-Binding Proteins/metabolism ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; In Vitro Techniques ; Myxovirus Resistance Proteins ; Papain ; Protein Binding ; Protein Conformation ; Proteins/chemistry ; Proteins/metabolism ; Recombinant Proteins/chemistry ; Recombinant Proteins/metabolism ; Trypsin
Chemical Substances	Antiviral Agents ; Myxovirus Resistance Proteins ; Proteins ; Recombinant Proteins ; Guanosine Diphosphate (146-91-8) ; Guanosine Triphosphate (86-01-1) ; Trypsin (EC 3.4.21.4) ; Endopeptidase K (EC 3.4.21.64) ; Papain (EC 3.4.22.2) ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2001-12-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/s0014-5793(02)02519-x
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Article: Dynamin interacts with members of the sumoylation machinery.

Mishra, Ram Kumar / Jatiani, Shashidhar S / Kumar, Ashutosh / Simhadri, Venkateswara Rao / Hosur, Ramakrishna V / Mittal, Rohit

The Journal of biological chemistry

2004 Volume 279, Issue 30, Page(s) 31445–31454

Abstract: Dynamin is a GTP-binding protein whose oligomerization-dependent assembly around the necks of lipid vesicles mediates their scission from parent membranes. Dynamin is thus directly involved in the regulation of endocytosis. Sumoylation is a post- ... ...

Abstract	Dynamin is a GTP-binding protein whose oligomerization-dependent assembly around the necks of lipid vesicles mediates their scission from parent membranes. Dynamin is thus directly involved in the regulation of endocytosis. Sumoylation is a post-translational protein modification whereby the ubiquitin-like modifier Sumo is covalently attached to lysine residues on target proteins by a process requiring the concerted action of an activating enzyme (ubiquitin-activating enzyme), a conjugating enzyme (ubiquitin carrier protein), and a ligating enzyme (ubiquitin-protein isopeptide ligase). Here, we show that dynamin interacts with Sumo-1, Ubc9, and PIAS-1, all of which are members of the sumoylation machinery. Ubc9 and PIAS-1 are known ubiquitin carrier protein and ubiquitin-protein isopeptide ligase enzymes, respectively, for the process of sumoylation. We have identified the coiled-coil GTPase effector domain (GED) of dynamin as the site on dynamin that interacts with Sumo-1, Ubc9, and PIAS-1. Although we saw no evidence of covalent Sumo-1 attachment to dynamin, Sumo-1 and Ubc9 are shown here to inhibit the lipid-dependent oligomerization of dynamin. Expression of Sumo-1 and Ubc9 in mammalian cells down-regulated the dynamin-mediated endocytosis of transferrin, whereas dynamin-independent fluid-phase uptake was not affected. Furthermore, using high resolution NMR spectroscopy, we have identified amino acid residues on Sumo-1 that directly interact with the GED of dynamin. The results suggest that the GED of dynamin may serve as a scaffold that concentrates the sumoylation machinery in the vicinity of potential acceptor proteins.
MeSH term(s)	Animals ; Base Sequence ; Binding Sites ; CHO Cells ; Carrier Proteins/chemistry ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cricetinae ; DNA Primers/genetics ; Dynamin I/chemistry ; Dynamin I/genetics ; Dynamin I/metabolism ; Humans ; In Vitro Techniques ; Kinetics ; Models, Molecular ; Protein Inhibitors of Activated STAT ; Protein Structure, Tertiary ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; SUMO-1 Protein/chemistry ; SUMO-1 Protein/genetics ; SUMO-1 Protein/metabolism ; Small Ubiquitin-Related Modifier Proteins/chemistry ; Small Ubiquitin-Related Modifier Proteins/genetics ; Small Ubiquitin-Related Modifier Proteins/metabolism ; Two-Hybrid System Techniques ; Ubiquitin-Conjugating Enzymes/chemistry ; Ubiquitin-Conjugating Enzymes/genetics ; Ubiquitin-Conjugating Enzymes/metabolism
Chemical Substances	Carrier Proteins ; DNA Primers ; PIAS1 protein, human ; Protein Inhibitors of Activated STAT ; Recombinant Proteins ; SUMO-1 Protein ; Small Ubiquitin-Related Modifier Proteins ; Ubiquitin-Conjugating Enzymes (EC 2.3.2.23) ; Dynamin I (EC 3.5.1.50) ; ubiquitin-conjugating enzyme UBC9 (EC 6.3.2.-)
Language	English
Publishing date	2004-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M402911200
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Article ; Online: A Non-ATP-Competitive Dual Inhibitor of JAK2 and BCR-ABL Kinases: Elucidation of a Novel Therapeutic Spectrum Based on Substrate Competitive Inhibition.

Jatiani, Shashidhar S / Cosenza, Stephen C / Reddy, M V Ramana / Ha, Ji Hee / Baker, Stacey J / Samanta, Ajoy K / Olnes, Matthew J / Pfannes, Loretta / Sloand, Elaine M / Arlinghaus, Ralph B / Reddy, E Premkumar

Genes & cancer

2010 Volume 1, Issue 4, Page(s) 331–345

Abstract: Here we report the discovery of ON044580, an α-benzoyl styryl benzyl sulfide that possesses potent inhibitory activity against two unrelated kinases, JAK2 and BCR-ABL, and exhibits cytotoxicity to human tumor cells derived from chronic myelogenous ... ...

Abstract	Here we report the discovery of ON044580, an α-benzoyl styryl benzyl sulfide that possesses potent inhibitory activity against two unrelated kinases, JAK2 and BCR-ABL, and exhibits cytotoxicity to human tumor cells derived from chronic myelogenous leukemia (CML) and myelodysplasia (MDS) patients or cells harboring a mutant JAK2 kinase. This novel spectrum of activity is explained by the non-ATP-competitive inhibition of JAK2 and BCR-ABL kinases. ON044580 inhibits mutant JAK2 kinase and the proliferation of JAK2(V617F)-positive leukemic cells and blocks the IL-3-mediated phosphorylation of JAK2 and STAT5. Interestingly, this compound also directly inhibits the kinase activity of both wild-type and imatinib-resistant (T315I) forms of the BCR-ABL kinase. Finally, ON044580 effectively induces apoptosis of imatinib-resistant CML patient cells. The apparently unrelated JAK2 and BCR-ABL kinases share a common substrate, STAT5, and such substrate competitive inhibitors represent an alternative therapeutic strategy for development of new inhibitors. The novel mechanism of kinase inhibition exhibited by ON044580 renders it effective against mutant forms of kinases such as the BCR-ABL(T315I) and JAK2(V617F). Importantly, ON044580 selectively reduces the number of aneuploid cells in primary bone marrow samples from monosomy 7 MDS patients, suggesting another regulatory cascade amenable to this agent in these aberrant cells. Data presented suggest that this compound could have multiple therapeutic applications including monosomy 7 MDS, imatinib-resistant CML, and myeloproliferative neoplasms that develop resistance to ATP-competitive agents.
Language	English
Publishing date	2010-05-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2538519-7
ISSN	1947-6027 ; 1947-6019
ISSN (online)	1947-6027
ISSN	1947-6019
DOI	10.1177/1947601910371337
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Article ; Online: Design, synthesis and evaluation of (E)-alpha-benzylthio chalcones as novel inhibitors of BCR-ABL kinase.

Reddy, M V Ramana / Pallela, Venkat R / Cosenza, Stephen C / Mallireddigari, Muralidhar R / Patti, Revathi / Bonagura, Marie / Truongcao, May / Akula, Balaiah / Jatiani, Shashidhar S / Reddy, E Premkumar

Bioorganic & medicinal chemistry

2010 Volume 18, Issue 6, Page(s) 2317–2326

Abstract: Novel (E)-alpha-benzylthio chalcones are reported with preliminary in vitro activity data indicating that several of them are potent inhibitors (comparable to imatinib, the reference compound) of BCR-ABL phosphorylation in leukemic K562 cells, known to ... ...

Abstract	Novel (E)-alpha-benzylthio chalcones are reported with preliminary in vitro activity data indicating that several of them are potent inhibitors (comparable to imatinib, the reference compound) of BCR-ABL phosphorylation in leukemic K562 cells, known to express high levels of BCR-ABL. The ability of such compounds to significantly inhibit K562 cell proliferation suggests that this scaffold could be a promising lead for the development of anticancer agents that are able to block BCR-ABL phosphorylation in leukemic cells.
MeSH term(s)	Cell Proliferation/drug effects ; Chalcones/chemical synthesis ; Chalcones/chemistry ; Chalcones/pharmacology ; Dose-Response Relationship, Drug ; Drug Design ; Drug Screening Assays, Antitumor ; Fusion Proteins, bcr-abl/antagonists & inhibitors ; Fusion Proteins, bcr-abl/metabolism ; Humans ; K562 Cells ; Molecular Structure ; Phosphorylation ; Protein Kinase Inhibitors/chemical synthesis ; Protein Kinase Inhibitors/chemistry ; Protein Kinase Inhibitors/pharmacology ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Protein-Tyrosine Kinases/metabolism ; Stereoisomerism ; Structure-Activity Relationship ; Tumor Cells, Cultured
Chemical Substances	(E)-alpha-benzylthio chalcone ; Chalcones ; Protein Kinase Inhibitors ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Fusion Proteins, bcr-abl (EC 2.7.10.2)
Language	English
Publishing date	2010-01-25
Publishing country	England
Document type	Evaluation Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1161284-8
ISSN	1464-3391 ; 0968-0896
ISSN (online)	1464-3391
ISSN	0968-0896
DOI	10.1016/j.bmc.2010.01.051
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Article ; Online: Discovery of 2-(1H-indol-5-ylamino)-6-(2,4-difluorophenylsulfonyl)-8-methylpyrido[2,3-d]pyrimidin-7(8H)-one (7ao) as a potent selective inhibitor of Polo like kinase 2 (PLK2).

Reddy, M V Ramana / Akula, Balireddy / Jatiani, Shashidhar / Vasquez-Del Carpio, Rodrigo / Billa, Vinay K / Mallireddigari, Muralidhar R / Cosenza, Stephen C / Venkata Subbaiah, D R C / Bharathi, E Vijaya / Pallela, Venkat R / Ramkumar, Poornima / Jain, Rinku / Aggarwal, Aneel K / Reddy, E Premkumar

Bioorganic & medicinal chemistry

2015 Volume 24, Issue 4, Page(s) 521–544

Abstract: Several families of protein kinases have been shown to play a critical role in the regulation of cell cycle progression, particularly progression through mitosis. These kinase families include the Aurora kinases, the Mps1 gene product and the Polo Like ... ...

Abstract	Several families of protein kinases have been shown to play a critical role in the regulation of cell cycle progression, particularly progression through mitosis. These kinase families include the Aurora kinases, the Mps1 gene product and the Polo Like family of protein kinases (PLKs). The PLK family consists of five members and of these, the role of PLK1 in human cancer is well documented. PLK2 (SNK), which is highly homologous to PLK1, has been shown to play a critical role in centriole duplication and is also believed to play a regulatory role in the survival pathway by physically stabilizing the TSC1/2 complex in tumor cells under hypoxic conditions. As a part of our research program, we have developed a library of novel ATP mimetic chemotypes that are cytotoxic against a panel of cancer cell lines. We show that one of these chemotypes, the 6-arylsulfonyl pyridopyrimidinones, induces apoptosis of human tumor cell lines in nanomolar concentrations. The most potent of these compounds, 7ao, was found to be a highly specific inhibitor of PLK2 when profiled against a panel of 288 wild type, 55 mutant and 12 lipid kinases. Here, we describe the synthesis, structure activity relationship, in vitro kinase specificity and biological activity of the lead compound, 7ao.
MeSH term(s)	Dose-Response Relationship, Drug ; Drug Discovery ; Humans ; Indoles/chemical synthesis ; Indoles/chemistry ; Indoles/pharmacology ; Molecular Structure ; Protein Kinase Inhibitors/chemical synthesis ; Protein Kinase Inhibitors/chemistry ; Protein Kinase Inhibitors/pharmacology ; Protein Serine-Threonine Kinases/antagonists & inhibitors ; Protein Serine-Threonine Kinases/metabolism ; Pyrimidinones/chemical synthesis ; Pyrimidinones/chemistry ; Pyrimidinones/pharmacology ; Structure-Activity Relationship
Chemical Substances	2-(1H-indol-5-ylamino)-6-(2,4-difluorophenylsulfonyl)-8-methylpyrido(2,3-d)pyrimidin-7(8H)-one ; Indoles ; Protein Kinase Inhibitors ; Pyrimidinones ; PLK2 protein, human (EC 2.7.11.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2015-12-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1161284-8
ISSN	1464-3391 ; 0968-0896
ISSN (online)	1464-3391
ISSN	0968-0896
DOI	10.1016/j.bmc.2015.11.045
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In stock of ZB MED Cologne/Königswinter

Order via subito