M Sattler

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi SHIP1, an SH2 domain containing polyinositol-5-phosphatase, regulates migration through two critical tyrosine residues and forms a novel signaling complex with DOK1 and CRKL
    M Sattler
    Dana Farber Cancer Institute, Department of Adult Oncology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 276:2451-8. 2001
  2. pmc BCR/ABL induces multiple abnormalities of cytoskeletal function
    R Salgia
    Division of Hematologic Malignancies, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Clin Invest 100:46-57. 1997
  3. ncbi p130CAS forms a signaling complex with the adapter protein CRKL in hematopoietic cells transformed by the BCR/ABL oncogene
    R Salgia
    Division of Hematologic Malignancies, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 271:25198-203. 1996
  4. ncbi 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
  5. ncbi The BCR/ABL oncogene alters interaction of the adapter proteins CRKL and CRK with cellular proteins
    N Uemura
    Division of Hematologic Malignancies, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Leukemia 11:376-85. 1997
  6. ncbi 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
  7. pmc BCR/ABL directly inhibits expression of SHIP, an SH2-containing polyinositol-5-phosphatase involved in the regulation of hematopoiesis
    M Sattler
    Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Mol Cell Biol 19:7473-80. 1999
  8. ncbi p210BCR/ABL induces formation of complexes containing focal adhesion proteins and the protooncogene product p120c-Cbl
    R Salgia
    Division of Hematologic Malignacies, Dana Farber Cancer Institute, Boston, MA 02115
    Exp Hematol 24:310-3. 1996
  9. ncbi 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 cells
    S N Manie
    Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 272:4230-6. 1997
  10. ncbi 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 factors
    M Sattler
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Oncogene 15:2379-84. 1997

Collaborators

Detail Information

Publications29

  1. ncbi SHIP1, an SH2 domain containing polyinositol-5-phosphatase, regulates migration through two critical tyrosine residues and forms a novel signaling complex with DOK1 and CRKL
    M 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...
  2. pmc BCR/ABL induces multiple abnormalities of cytoskeletal function
    R 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...
  3. ncbi p130CAS forms a signaling complex with the adapter protein CRKL in hematopoietic cells transformed by the BCR/ABL oncogene
    R 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...
  4. ncbi 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...
  5. ncbi The BCR/ABL oncogene alters interaction of the adapter proteins CRKL and CRK with cellular proteins
    N 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...
  6. ncbi 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...
  7. pmc BCR/ABL directly inhibits expression of SHIP, an SH2-containing polyinositol-5-phosphatase involved in the regulation of hematopoiesis
    M 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...
  8. ncbi p210BCR/ABL induces formation of complexes containing focal adhesion proteins and the protooncogene product p120c-Cbl
    R 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...
  9. ncbi 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 cells
    S 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...
  10. ncbi 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 factors
    M 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...
  11. ncbi Activation of hematopoietic growth factor signal transduction pathways by the human oncogene BCR/ABL
    M 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...
  12. ncbi The BCR/ABL tyrosine kinase induces production of reactive oxygen species in hematopoietic cells
    M 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...
  13. pmc The JAK2V617F oncogene requires expression of inducible phosphofructokinase/fructose-bisphosphatase 3 for cell growth and increased metabolic activity
    M 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...
  14. ncbi Mechanisms of transformation by the BCR/ABL oncogene
    M 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...
  15. ncbi Thrombopoietin induces activation of the phosphatidylinositol-3' kinase pathway and formation of a complex containing p85PI3K and the protooncoprotein p120CBL
    M 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...
  16. doi Kinase domain mutations confer resistance to novel inhibitors targeting JAK2V617F in myeloproliferative neoplasms
    A 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...
  17. ncbi CRKL links p210BCR/ABL with paxillin in chronic myelogenous leukemia cells
    R 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...
  18. doi Using combination therapy to override stromal-mediated chemoresistance in mutant FLT3-positive AML: synergism between FLT3 inhibitors, dasatinib/multi-targeted inhibitors and JAK inhibitors
    E 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...
  19. ncbi The BCR/ABL oncogene alters the chemotactic response to stromal-derived factor-1alpha
    R Salgia
    Department of Medical Oncology, Division of Hematologic Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
    Blood 94:4233-46. 1999
    ....
  20. doi NADPH oxidases regulate cell growth and migration in myeloid cells transformed by oncogenic tyrosine kinases
    M 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...
  21. ncbi Vascular endothelial growth factor triggers signaling cascades mediating multiple myeloma cell growth and migration
    K 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...
  22. doi Drug resistance in mutant FLT3-positive AML
    E Weisberg
    Department of Medical Oncology Hematologic Neoplasia, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
    Oncogene 29:5120-34. 2010
    ....
  23. ncbi Structure and ligand recognition of the phosphotyrosine binding domain of Shc
    M 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...
  24. ncbi SMN tudor domain structure and its interaction with the Sm proteins
    P 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...
  25. doi A structure refinement protocol combining NMR residual dipolar couplings and small angle scattering restraints
    F Gabel
    Structural and Computational Biology Unit, EMBL, Meyerhofstrasse 1, Heidelberg, Germany
    J Biomol NMR 41:199-208. 2008
    ....
  26. ncbi Structural basis for recognition of the intron branch site RNA by splicing factor 1
    Z 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...
  27. ncbi The SAND domain structure defines a novel DNA-binding fold in transcriptional regulation
    M 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...
  28. pmc Prediction of structural domains of TAP reveals details of its interaction with p15 and nucleoporins
    M 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...
  29. ncbi Refinement of the protein backbone angle psi in NMR structure calculations
    R 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...