Research Topics
Genomes and Genes
| M SattlerSummaryAffiliation: Harvard University Country: USA Publications
| Collaborators
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Detail Information
Publications
SHIP1, an SH2 domain containing polyinositol-5-phosphatase, regulates migration through two critical tyrosine residues and forms a novel signaling complex with DOK1 and CRKLM Sattler
Dana Farber Cancer Institute, Department of Adult Oncology, Harvard Medical School, Boston, Massachusetts 02115, USA
J Biol Chem 276:2451-8. 2001..Overall, these data suggest that proteins that interact with SHIP1 through Tyr(917) and Tyr(1020), such as DOK1 and SHC, are likely to be involved in the regulation of SHIP1 dependent migration...
BCR/ABL induces multiple abnormalities of cytoskeletal functionR Salgia
Division of Hematologic Malignancies, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
J Clin Invest 100:46-57. 1997..The increase in spontaneous motility and other defects of cytoskeletal function described here will be useful biological markers of the functional effects of BCR/ABL in hematopoietic cells...- p130CAS forms a signaling complex with the adapter protein CRKL in hematopoietic cells transformed by the BCR/ABL oncogeneR Salgia
Division of Hematologic Malignancies, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
J Biol Chem 271:25198-203. 1996..These alterations in the structure of signaling proteins in focal adhesion like structures could contribute to the known adhesion abnormalities in CML cells... - Steel factor induces tyrosine phosphorylation of CRKL and binding of CRKL to a complex containing c-kit, phosphatidylinositol 3-kinase, and p120(CBL)M Sattler
Division of Hematologic Malignancies, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
J Biol Chem 272:10248-53. 1997..Such complexes could be important in propagating signals involving PI3K such as gene expression and adhesion... - Differential signaling after beta1 integrin ligation is mediated through binding of CRKL to p120(CBL) and p110(HEF1)M Sattler
Division of Hematologic Malignancies, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
J Biol Chem 272:14320-6. 1997..The shift in association of CRKL and its SH3-associated proteins from p120(CBL) to p110(HEF1) could contribute to different functional outcomes of "outside-in" integrin signaling in different cells... - The BCR/ABL oncogene alters interaction of the adapter proteins CRKL and CRK with cellular proteinsN Uemura
Division of Hematologic Malignancies, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Leukemia 11:376-85. 1997..In BCR/ABL-transformed cells, CRKL but not CRK II, appears to form complexes which potentially link BCR/ABL, c-ABL, C3G, and SOS to the protooncoprotein, p120CBL... - p210BCR/ABL induces formation of complexes containing focal adhesion proteins and the protooncogene product p120c-CblR Salgia
Division of Hematologic Malignacies, Dana Farber Cancer Institute, Boston, MA 02115
Exp Hematol 24:310-3. 1996..The binding of p120c-Cbl to the focal adhesion protein paxillin could contribute to the known adhesive defects of CML cells... - BCR/ABL directly inhibits expression of SHIP, an SH2-containing polyinositol-5-phosphatase involved in the regulation of hematopoiesisM Sattler
Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Mol Cell Biol 19:7473-80. 1999..Reexpression of SHIP in BCR/ABL-transformed Ba/F3 cells altered the biological behavior of cells in culture. The reduction of SHIP due to BCR/ABL is likely to directly contribute to the pathogenesis of CML... - Involvement of p130(Cas) and p105(HEF1), a novel Cas-like docking protein, in a cytoskeleton-dependent signaling pathway initiated by ligation of integrin or antigen receptor on human B cellsS N Manie
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
J Biol Chem 272:4230-6. 1997..These associations implicate HEF1 and Cas as important components in a cytoskeleton-linked signaling pathway initiated by ligation of beta1 integrin or BCR on human B cells... - The BCR/ABL tyrosine kinase induces production of reactive oxygen species in hematopoietic cellsM Sattler
Dana Farber Cancer Institute, Department of Adult Oncology, Harvard Medical School, Boston, Massachusetts 02115, USA
J Biol Chem 275:24273-8. 2000..Further, treatment of MO7e cells with H(2)O(2) or pervanadate increased the tyrosine kinase activity of c-ABL. Drugs that alter ROS metabolism or reactivate PTPases may antagonize BCR/ABL transformation... - Activation of hematopoietic growth factor signal transduction pathways by the human oncogene BCR/ABLM Sattler
Division of Hematologic Malignancies, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cytokine Growth Factor Rev 8:63-79. 1997..In this review, we will describe the molecular and biological abnormalities in CML and several signal transduction mechanisms utilized by BCR/ABL as compared to hematopoietic growth factors... - The phosphatidylinositol polyphosphate 5-phosphatase SHIP and the protein tyrosine phosphatase SHP-2 form a complex in hematopoietic cells which can be regulated by BCR/ABL and growth factorsM Sattler
Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Oncogene 15:2379-84. 1997..These data suggest that the function of SHIP and SHP-2 in normal cells are linked and that BCR/ABL alters the function of this signaling complex... - The JAK2V617F oncogene requires expression of inducible phosphofructokinase/fructose-bisphosphatase 3 for cell growth and increased metabolic activityM M Reddy
Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA, USA
Leukemia 26:481-9. 2012..Novel therapies that specifically block PFKFB3 activity or expression would, therefore, be expected to inhibit JAK2/STAT5-dependent malignancies and related cancers... - Mechanisms of transformation by the BCR/ABL oncogeneM Sattler
Department of Adult Oncology, Dana-Farber Cancer Institute, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
Int J Hematol 73:278-91. 2001..This review will describe mechanisms of transformation by the BCR/ABL oncogene and opportunities for clinical intervention with specific signal transduction inhibitors such as STI-571 in CML... - Thrombopoietin induces activation of the phosphatidylinositol-3' kinase pathway and formation of a complex containing p85PI3K and the protooncoprotein p120CBLM Sattler
Division of Hematologic Malignancies, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
J Cell Physiol 171:28-33. 1997..p120CBL may be involved in signaling pathways activated by c-MPL which involve phosphatidylinositol-3' kinase... 
Kinase domain mutations confer resistance to novel inhibitors targeting JAK2V617F in myeloproliferative neoplasmsA Deshpande
Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA, USA
Leukemia 26:708-15. 2012..These results suggest that JAK2 inhibitors currently in clinical trials may be prone to resistance as a result of point mutations and caution should be exercised when administering these drugs...- CRKL links p210BCR/ABL with paxillin in chronic myelogenous leukemia cellsR Salgia
Division of Hematologic Malignancies, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
J Biol Chem 270:29145-50. 1995..These results suggest that the p210BCR/ABL oncogene may be physically linked to the focal adhesion-associated protein paxillin in hematopoietic cells by CRKL. This interaction could contribute to the known adhesive defects of CML cells... - Using combination therapy to override stromal-mediated chemoresistance in mutant FLT3-positive AML: synergism between FLT3 inhibitors, dasatinib/multi-targeted inhibitors and JAK inhibitorsE Weisberg
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
Leukemia 26:2233-44. 2012..These results hint at a novel concept of using combination therapy to override drug resistance in mutant FLT3-positive AML in the bone marrow niche and suppress or eradicate residual disease... - The BCR/ABL oncogene alters the chemotactic response to stromal-derived factor-1alphaR Salgia
Department of Medical Oncology, Division of Hematologic Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
Blood 94:4233-46. 1999.... - NADPH oxidases regulate cell growth and migration in myeloid cells transformed by oncogenic tyrosine kinasesM M Reddy
Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA, USA
Leukemia 25:281-9. 2011..MARCKS was also found to be required for increased migration. Overall, these data suggest a model whereby NOX links metabolic NADPH production to cellular events that directly contribute to transformation... - Vascular endothelial growth factor triggers signaling cascades mediating multiple myeloma cell growth and migrationK Podar
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
Blood 98:428-35. 2001..These observations provide the framework for novel therapeutic strategies targeting VEGF signaling cascades in MM... - Drug resistance in mutant FLT3-positive AMLE Weisberg
Department of Medical Oncology Hematologic Neoplasia, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
Oncogene 29:5120-34. 2010.... - Structure and ligand recognition of the phosphotyrosine binding domain of ShcM M Zhou
Pharmaceutical Discovery Division, Abbott Laboratories, Abbott Park, Illinois 60064, USA
Nature 378:584-92. 1995..The PTB domain is structurally similar to pleckstrin homology domains (a beta-sandwich capped by an alpha-helix) and binds to acidic phospholipids, suggesting a possible role in membrane localization... - SMN tudor domain structure and its interaction with the Sm proteinsP Selenko
Structural and Computational Biology, EMBL, Meyerhofstr 1, D 69012 Heidelberg, Germany
Nat Struct Biol 8:27-31. 2001..Our data provide a structural basis for a molecular defect underlying SMA... - A structure refinement protocol combining NMR residual dipolar couplings and small angle scattering restraintsF Gabel
Structural and Computational Biology Unit, EMBL, Meyerhofstrasse 1, Heidelberg, Germany
J Biomol NMR 41:199-208. 2008.... - Structural basis for recognition of the intron branch site RNA by splicing factor 1Z Liu
European Molecular Biology Laboratory EMBL, Meyerhofstrasse 1, D 69117 Heidelberg, Germany
Science 294:1098-102. 2001..The branch point adenosine acting as the nucleophile in the first biochemical step of splicing is deeply buried. BPS RNA recognition suggests how SF1 may facilitate subsequent formation of the prespliceosomal complex A... - The SAND domain structure defines a novel DNA-binding fold in transcriptional regulationM J Bottomley
European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany
Nat Struct Biol 8:626-33. 2001..The evolutionarily conserved SAND domain defines a new DNA binding fold that is involved in chromatin-associated transcriptional regulation... - Prediction of structural domains of TAP reveals details of its interaction with p15 and nucleoporinsM Suyama
EMBL, Heidelberg, Germany
EMBO Rep 1:53-8. 2000..Furthermore, the C-terminus of TAP was found to contain a ubiquitin-associated (UBA) domain. By site-directed mutagenesis we show that a conserved loop in this domain plays an essential role in mediating TAP-nucleoporin interaction... - Refinement of the protein backbone angle psi in NMR structure calculationsR Sprangers
European Molecular Biology Laboratory, Heidelberg, Germany
J Biomol NMR 16:47-58. 2000..8 A crystal structure, suggesting an improved accuracy. The proposed refinement method can be used to significantly improve the quality of NMR structures and will be applicable to larger proteins...