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Article ; Online: Stem cells: Dual response to Ras mutation.

Chu, S Haihua / Armstrong, Scott A

2013 Volume 504, Issue 7478, Page(s) 91–92

MeSH term(s)	Animals ; Genes, ras/genetics ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism
Language	English
Publishing date	2013-11-27
Publishing country	England
Document type	News ; Comment
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/nature12840
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Zs.A 26: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Mechanisms of resistance to FLT3 inhibitors.

Chu, S Haihua / Small, Donald

Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy

2009 Volume 12, Issue 1-2, Page(s) 8–16

Abstract: The success of the small molecule tyrosine kinase receptor inhibitor (TKI) imatinib mesylate (Gleevec) in the treatment of chronic myeloid leukemia (CML) constitutes an eminent paradigm shift advocating the rational design of cancer therapeutics ... ...

Abstract	The success of the small molecule tyrosine kinase receptor inhibitor (TKI) imatinib mesylate (Gleevec) in the treatment of chronic myeloid leukemia (CML) constitutes an eminent paradigm shift advocating the rational design of cancer therapeutics specifically targeting the transformation events that drive tumorigenicity. In acute myeloid leukemias (AMLs), the most frequent identified transforming events are activating mutations in the FLT3 receptor tyrosine kinase that constitutively activate survival and proliferation pathways. FLT3 TKIs that are in various phases of clinical trials are showing some initial promise. However, primary and secondary acquired resistance stands to severely compromise long-term and durable efficacy of these inhibitors as a therapeutic strategy. Here, we discuss the mechanisms of resistance to FLT3 inhibitors and possible strategies to overcome resistance through closer examination of the events of leukemogenesis and design of combination therapy.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacokinetics ; Antineoplastic Agents/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Drug Resistance, Neoplasm/genetics ; Gene Expression Regulation, Leukemic ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/enzymology ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/pathology ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/enzymology ; Protein Kinase Inhibitors/pharmacokinetics ; Protein Kinase Inhibitors/therapeutic use ; fms-Like Tyrosine Kinase 3/antagonists & inhibitors ; fms-Like Tyrosine Kinase 3/genetics ; fms-Like Tyrosine Kinase 3/metabolism
Chemical Substances	Antineoplastic Agents ; Protein Kinase Inhibitors ; FLT3 protein, human (EC 2.7.10.1) ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1)
Language	English
Publishing date	2009-01-21
Publishing country	Scotland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1474513-6
ISSN	1532-2084 ; 1368-7646
ISSN (online)	1532-2084
ISSN	1368-7646
DOI	10.1016/j.drup.2008.12.001
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Article ; Online: miR-99 regulates normal and malignant hematopoietic stem cell self-renewal.

Khalaj, Mona / Woolthuis, Carolien M / Hu, Wenhuo / Durham, Benjamin H / Chu, S Haihua / Qamar, Sarah / Armstrong, Scott A / Park, Christopher Y

The Journal of experimental medicine

2018 Volume 214, Issue 8, Page(s) 2453–2470

Abstract: The microRNA-99 (miR-99) family comprises a group of broadly conserved microRNAs that are highly expressed in hematopoietic stem cells (HSCs) and acute myeloid leukemia stem cells (LSCs) compared with their differentiated progeny. Herein, we show that ... ...

Abstract	The microRNA-99 (miR-99) family comprises a group of broadly conserved microRNAs that are highly expressed in hematopoietic stem cells (HSCs) and acute myeloid leukemia stem cells (LSCs) compared with their differentiated progeny. Herein, we show that miR-99 regulates self-renewal in both HSCs and LSCs. miR-99 maintains HSC long-term reconstitution activity by inhibiting differentiation and cell cycle entry. Moreover, miR-99 inhibition induced LSC differentiation and depletion in an MLL-AF9-driven mouse model of AML, leading to reduction in leukemia-initiating activity and improved survival in secondary transplants. Confirming miR-99's role in established AML, miR-99 inhibition induced primary AML patient blasts to undergo differentiation. A forward genetic shRNA library screen revealed Hoxa1 as a critical mediator of miR-99 function in HSC maintenance, and this observation was independently confirmed in both HSCs and LSCs. Together, these studies demonstrate the importance of noncoding RNAs in the regulation of HSC and LSC function and identify miR-99 as a critical regulator of stem cell self-renewal.
MeSH term(s)	Animals ; Cell Cycle/genetics ; Cell Differentiation/genetics ; Cell Line, Tumor ; Cell Self Renewal/genetics ; Cell Self Renewal/physiology ; Hematopoietic Stem Cells/physiology ; Homeodomain Proteins/genetics ; Humans ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/pathology ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics ; RNA, Small Interfering/genetics ; Transcription Factors/genetics
Chemical Substances	Homeodomain Proteins ; MIRN99 microRNA, human ; MicroRNAs ; RNA, Small Interfering ; Transcription Factors ; homeobox A1 protein
Language	English
Publishing date	2018-04-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20161595
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Ua VI Zs.107: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Rationally Designed Base Editors for Precise Editing of the Sickle Cell Disease Mutation.

Chu, S Haihua / Packer, Michael / Rees, Holly / Lam, Dieter / Yu, Yi / Marshall, Jeffrey / Cheng, Lo-I / Lam, Daisy / Olins, Jenny / Ran, Fei Ann / Liquori, Alexander / Gantzer, Bob / Decker, Jeremy / Born, David / Barrera, Luis / Hartigan, Adam / Gaudelli, Nicole / Ciaramella, Giuseppe / Slaymaker, Ian M

The CRISPR journal

2021 Volume 4, Issue 2, Page(s) 169–177

Abstract: Base editors are fusions of a deaminase and CRISPR-Cas ribonucleoprotein that allow programmable installment of transition mutations without double-strand DNA break intermediates. The breadth of potential base editing targets is frequently limited by the ...

Abstract	Base editors are fusions of a deaminase and CRISPR-Cas ribonucleoprotein that allow programmable installment of transition mutations without double-strand DNA break intermediates. The breadth of potential base editing targets is frequently limited by the requirement of a suitably positioned Cas9 protospacer adjacent motif. To address this, we used structures of Cas9 and TadA to design a set of inlaid base editors (IBEs), in which deaminase domains are internal to Cas9. Several of these IBEs exhibit shifted editing windows and greater editing efficiency, enabling editing of targets outside the canonical editing window with reduced DNA and RNA off-target editing frequency. Finally, we show that IBEs enable conversion of the pathogenic sickle cell hemoglobin allele to the naturally occurring HbG-Makassar variant in patient-derived hematopoietic stem cells.
MeSH term(s)	Anemia, Sickle Cell/genetics ; Anemia, Sickle Cell/therapy ; CRISPR-Associated Protein 9 ; CRISPR-Cas Systems ; Clustered Regularly Interspaced Short Palindromic Repeats ; DNA ; DNA Breaks, Double-Stranded ; Gene Editing ; HEK293 Cells ; High-Throughput Nucleotide Sequencing ; Humans ; Mutation ; RNA
Chemical Substances	RNA (63231-63-0) ; DNA (9007-49-2) ; CRISPR-Associated Protein 9 (EC 3.1.-)
Language	English
Publishing date	2021-04-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	3017891-5
ISSN	2573-1602 ; 2573-1599
ISSN (online)	2573-1602
ISSN	2573-1599
DOI	10.1089/crispr.2020.0144
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Zs.MG 119: Show issues

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Article ; Online: Loss of H3K36 Methyltransferase SETD2 Impairs V(D)J Recombination during Lymphoid Development.

Chu, S Haihua / Chabon, Jonathan R / Matovina, Chloe N / Minehart, Janna C / Chen, Bo-Ruei / Zhang, Jian / Kumar, Vipul / Xiong, Yijun / Callen, Elsa / Hung, Putzer J / Feng, Zhaohui / Koche, Richard P / Liu, X Shirley / Chaudhuri, Jayanta / Nussenzweig, Andre / Sleckman, Barry P / Armstrong, Scott A

iScience

2020 Volume 23, Issue 3, Page(s) 100941

Abstract: Repair of DNA double-stranded breaks (DSBs) during lymphocyte development is essential for V(D)J recombination and forms the basis of immunoglobulin variable region diversity. Understanding of this process in lymphogenesis has historically been centered ... ...

Abstract	Repair of DNA double-stranded breaks (DSBs) during lymphocyte development is essential for V(D)J recombination and forms the basis of immunoglobulin variable region diversity. Understanding of this process in lymphogenesis has historically been centered on the study of RAG1/2 recombinases and a set of classical non-homologous end-joining factors. Much less has been reported regarding the role of chromatin modifications on this process. Here, we show a role for the non-redundant histone H3 lysine methyltransferase, Setd2, and its modification of lysine-36 trimethylation (H3K36me3), in the processing and joining of DNA ends during V(D)J recombination. Loss leads to mis-repair of Rag-induced DNA DSBs, especially when combined with loss of Atm kinase activity. Furthermore, loss reduces immune repertoire and a severe block in lymphogenesis as well as causes post-mitotic neuronal apoptosis. Together, these studies are suggestive of an important role of Setd2/H3K36me3 in these two mammalian developmental processes that are influenced by double-stranded break repair.
Language	English
Publishing date	2020-02-27
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2020.100941
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Article ; Online: Inhibition of MEK and ATR is effective in a B-cell acute lymphoblastic leukemia model driven by

Chu, S Haihua / Song, Evelyn J / Chabon, Jonathan R / Minehart, Janna / Matovina, Chloe N / Makofske, Jessica L / Frank, Elizabeth S / Ross, Kenneth / Koche, Richard P / Feng, Zhaohui / Xu, Haiming / Krivtsov, Andrei / Nussenzweig, Andre / Armstrong, Scott A

Blood advances

2018 Volume 2, Issue 19, Page(s) 2478–2490

Abstract: Infant B-cell acute lymphoblastic leukemias (B-ALLs) that ... ...

Abstract	Infant B-cell acute lymphoblastic leukemias (B-ALLs) that harbor
MeSH term(s)	Animals ; Apoptosis/genetics ; Ataxia Telangiectasia Mutated Proteins/antagonists & inhibitors ; Cell Cycle/genetics ; Disease Models, Animal ; Disease Progression ; Gene Expression ; Genes, ras ; Genetic Vectors/genetics ; Humans ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors ; Mutation ; Myeloid-Lymphoid Leukemia Protein/genetics ; Myeloid-Lymphoid Leukemia Protein/metabolism ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/metabolism ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Protein Kinase Inhibitors/pharmacology ; Retroviridae/genetics ; Signal Transduction ; Transcriptional Activation
Chemical Substances	MLL-AF4 fusion protein, human ; Oncogene Proteins, Fusion ; Protein Kinase Inhibitors ; Myeloid-Lymphoid Leukemia Protein (149025-06-9) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2018-09-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2018021592
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Article ; Online: Myeloid progenitor cluster formation drives emergency and leukaemic myelopoiesis.

Hérault, Aurélie / Binnewies, Mikhail / Leong, Stephanie / Calero-Nieto, Fernando J / Zhang, Si Yi / Kang, Yoon-A / Wang, Xiaonan / Pietras, Eric M / Chu, S Haihua / Barry-Holson, Keegan / Armstrong, Scott / Göttgens, Berthold / Passegué, Emmanuelle

Nature

2017 Volume 544, Issue 7648, Page(s) 53–58

Abstract: Although many aspects of blood production are well understood, the spatial organization of myeloid differentiation in the bone marrow remains unknown. Here we use imaging to track granulocyte/macrophage progenitor (GMP) behaviour in mice during emergency ...

Abstract	Although many aspects of blood production are well understood, the spatial organization of myeloid differentiation in the bone marrow remains unknown. Here we use imaging to track granulocyte/macrophage progenitor (GMP) behaviour in mice during emergency and leukaemic myelopoiesis. In the steady state, we find individual GMPs scattered throughout the bone marrow. During regeneration, we observe expanding GMP patches forming defined GMP clusters, which, in turn, locally differentiate into granulocytes. The timed release of important bone marrow niche signals (SCF, IL-1β, G-CSF, TGFβ and CXCL4) and activation of an inducible Irf8 and β-catenin progenitor self-renewal network control the transient formation of regenerating GMP clusters. In leukaemia, we show that GMP clusters are constantly produced owing to persistent activation of the self-renewal network and a lack of termination cytokines that normally restore haematopoietic stem-cell quiescence. Our results uncover a previously unrecognized dynamic behaviour of GMPs in situ, which tunes emergency myelopoiesis and is hijacked in leukaemia.
MeSH term(s)	Animals ; Cell Self Renewal ; Cellular Reprogramming ; Cytokines/metabolism ; Granulocyte-Macrophage Progenitor Cells/cytology ; Granulocyte-Macrophage Progenitor Cells/pathology ; Granulocytes/cytology ; Granulocytes/pathology ; Interferon Regulatory Factors/metabolism ; Leukemia/pathology ; Macrophages/cytology ; Macrophages/pathology ; Mice ; Molecular Imaging ; Myelopoiesis ; Neoplastic Stem Cells/pathology ; Stem Cell Niche/physiology ; beta Catenin/metabolism
Chemical Substances	Cytokines ; Interferon Regulatory Factors ; beta Catenin ; interferon regulatory factor-8
Language	English
Publishing date	2017-03-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/nature21693
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Article: Polyhydroxybutyrate-enhanced transformation of log-phase Escherichia coli.

Addison, Charles J / Chu, S Haihua / Reusch, Rosetta N

BioTechniques

2004 Volume 37, Issue 3, Page(s) 376–8, 380, 382

Abstract: Transformation of Escherichia coli plays an important role in recombinant DNA technology. Most current transformation protocols require that the cells be treated to attain a particular physiological state known as "competence," and this makes ... ...

Abstract	Transformation of Escherichia coli plays an important role in recombinant DNA technology. Most current transformation protocols require that the cells be treated to attain a particular physiological state known as "competence," and this makes transformation procedures lengthy and arduous. Here we describe a protocol for transforming log-phase E. coli using dimethyl sulfoxide (DMSO) solutions of poly-(R)-3-hydroxybutyrate (PHB) to facilitate the transfer of plasmid DNA into cells, and certain reagents and temperature shocks to promote DNA uptake. The protocol was optimized using factorial design techniques across variables that included PHB molecular weight and concentration, DMSO concentration, monovalent and divalent salts, glucose, cold and heat shocks, cell density, and pH. Using 10 ng DNA, the optimized protocol produces approximately 1000 colony-forming units (CFUs) from 100 microL early log-phase cell culture or approximately 300 CFU from a 21-24 h single colony, sufficient for many applications. The total volume of the transformation reaction mixture is only 150 microL suggesting that the procedure may be adapted for use in microplates or automated transformation technologies.
MeSH term(s)	DNA, Bacterial ; Escherichia coli/genetics ; Escherichia coli/metabolism ; Hydroxybutyrates ; Indicators and Reagents ; Plasmids ; Polyesters ; Recombination, Genetic ; Transformation, Bacterial
Chemical Substances	DNA, Bacterial ; Hydroxybutyrates ; Indicators and Reagents ; Polyesters ; poly-beta-hydroxybutyrate (26063-00-3)
Language	English
Publishing date	2004-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Technical Report
ZDB-ID	48453-2
ISSN	1940-9818 ; 0736-6205
ISSN (online)	1940-9818
ISSN	0736-6205
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Article ; Online: NUP98 Fusion Proteins Interact with the NSL and MLL1 Complexes to Drive Leukemogenesis.

Xu, Haiming / Valerio, Daria G / Eisold, Meghan E / Sinha, Amit / Koche, Richard P / Hu, Wenhuo / Chen, Chun-Wei / Chu, S Haihua / Brien, Gerard L / Park, Christopher Y / Hsieh, James J / Ernst, Patricia / Armstrong, Scott A

Cancer cell

2016 Volume 30, Issue 6, Page(s) 863–878

Abstract: The nucleoporin 98 gene (NUP98) is fused to a variety of partner genes in multiple hematopoietic malignancies. Here, we demonstrate that NUP98 fusion proteins, including NUP98-HOXA9 (NHA9), NUP98-HOXD13 (NHD13), NUP98-NSD1, NUP98-PHF23, and NUP98-TOP1 ... ...

Abstract	The nucleoporin 98 gene (NUP98) is fused to a variety of partner genes in multiple hematopoietic malignancies. Here, we demonstrate that NUP98 fusion proteins, including NUP98-HOXA9 (NHA9), NUP98-HOXD13 (NHD13), NUP98-NSD1, NUP98-PHF23, and NUP98-TOP1 physically interact with mixed lineage leukemia 1 (MLL1) and the non-specific lethal (NSL) histone-modifying complexes. Chromatin immunoprecipitation sequencing illustrates that NHA9 and MLL1 co-localize on chromatin and are found associated with Hox gene promoter regions. Furthermore, MLL1 is required for the proliferation of NHA9 cells in vitro and in vivo. Inactivation of MLL1 leads to decreased expression of genes bound by NHA9 and MLL1 and reverses a gene expression signature found in NUP98-rearranged human leukemias. Our data reveal a molecular dependency on MLL1 function in NUP98-fusion-driven leukemogenesis.
MeSH term(s)	Animals ; Cell Proliferation ; Chromatin/metabolism ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Histone-Lysine N-Methyltransferase/metabolism ; Homeodomain Proteins/genetics ; Humans ; Leukemia/metabolism ; Mice ; Myeloid-Lymphoid Leukemia Protein/metabolism ; Nuclear Pore Complex Proteins/genetics ; Nuclear Pore Complex Proteins/metabolism ; Oncogene Proteins, Fusion/metabolism ; Promoter Regions, Genetic ; Tumor Cells, Cultured
Chemical Substances	Chromatin ; Homeodomain Proteins ; Nuclear Pore Complex Proteins ; Oncogene Proteins, Fusion ; nuclear pore complex protein 98 ; Myeloid-Lymphoid Leukemia Protein (149025-06-9) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; Kmt2a protein, mouse (EC 2.1.1.43)
Language	English
Publishing date	2016-11-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2016.10.019
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Article ; Online: Resistance Mechanisms to SYK Inhibition in Acute Myeloid Leukemia.

Cremer, Anjali / Ellegast, Jana M / Alexe, Gabriela / Frank, Elizabeth S / Ross, Linda / Chu, S Haihua / Pikman, Yana / Robichaud, Amanda / Goodale, Amy / Häupl, Björn / Mohr, Sebastian / Rao, Arati V / Walker, Alison R / Blachly, James S / Piccioni, Federica / Armstrong, Scott A / Byrd, John C / Oellerich, Thomas / Stegmaier, Kimberly

Cancer discovery

2019 Volume 10, Issue 2, Page(s) 214–231

Abstract: Spleen tyrosine kinase (SYK) is a nonmutated therapeutic target in acute myeloid leukemia (AML). Attempts to exploit SYK therapeutically in AML have shown promising results in combination with chemotherapy, likely reflecting induced mechanisms of ... ...

Abstract	Spleen tyrosine kinase (SYK) is a nonmutated therapeutic target in acute myeloid leukemia (AML). Attempts to exploit SYK therapeutically in AML have shown promising results in combination with chemotherapy, likely reflecting induced mechanisms of resistance to single-agent treatment
MeSH term(s)	Animals ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Benzamides/pharmacology ; Benzamides/therapeutic use ; Cell Line, Tumor ; Clinical Trials, Phase I as Topic ; Clinical Trials, Phase II as Topic ; Diphenylamine/analogs & derivatives ; Diphenylamine/pharmacology ; Diphenylamine/therapeutic use ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Drug Synergism ; Female ; Gene Expression Regulation, Leukemic/drug effects ; Humans ; Indazoles/pharmacology ; Indazoles/therapeutic use ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; MAP Kinase Signaling System/drug effects ; MAP Kinase Signaling System/genetics ; Mice ; Mitogen-Activated Protein Kinase 1/genetics ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Mutagenesis, Site-Directed ; Mutation ; Open Reading Frames/genetics ; Primary Cell Culture ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Protein Tyrosine Phosphatase, Non-Receptor Type 11/genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 11/metabolism ; Pyrazines/pharmacology ; Pyrazines/therapeutic use ; Syk Kinase/antagonists & inhibitors ; Syk Kinase/metabolism ; Xenograft Model Antitumor Assays
Chemical Substances	6-(1H-indazol-6-yl)-N-(4-morpholinophenyl)imidazo(1,2-a)pyrazin-8-amine ; Benzamides ; Indazoles ; Protein Kinase Inhibitors ; Pyrazines ; mirdametinib (86K0J5AK6M) ; Diphenylamine (9N3CBB0BIQ) ; SYK protein, human (EC 2.7.10.2) ; Syk Kinase (EC 2.7.10.2) ; MAPK1 protein, human (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; PTPN11 protein, human (EC 3.1.3.48) ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 (EC 3.1.3.48)
Language	English
Publishing date	2019-11-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-19-0209
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