Jean Y Wang

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Induction of cell retraction by the combined actions of Abl-CrkII and Rho-ROCK1 signaling
    Xiaodong Huang
    Division of Biological Sciences, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA
    J Cell Biol 183:711-23. 2008
  2. pmc Persistent inhibition of ABL tyrosine kinase causes enhanced apoptotic response to TRAIL and disrupts the pro-apoptotic effect of chloroquine
    Priya Sridevi
    Moores Cancer Center, Division of Hematology Oncology, Department of Medicine, School of Medicine, University of California San Diego, La Jolla, California, United States of America
    PLoS ONE 8:e77495. 2013
  3. pmc Separation of anti-proliferation and anti-apoptotic functions of retinoblastoma protein through targeted mutations of its A/B domain
    B Nelson Chau
    Department of Medicine, Division of Hematology Oncology, Moores UCSD Cancer Center, University of California San Diego, La Jolla, California, United States of America
    PLoS ONE 1:e82. 2006
  4. pmc Interplay between kinase domain autophosphorylation and F-actin binding domain in regulating imatinib sensitivity and nuclear import of BCR-ABL
    Martin Preyer
    Division of Hematology Oncology and Moores Cancer Center, Department of Medicine, University of California San Diego School of Medicine, La Jolla, California, United States of America
    PLoS ONE 6:e17020. 2011
  5. pmc Genetic disruption of Abl nuclear import reduces renal apoptosis in a mouse model of cisplatin-induced nephrotoxicity
    P Sridevi
    Division of Hematology Oncology, Department of Medicine, Moores UCSD Cancer Center, UCSD School of Medicine, University of California, San Diego, La Jolla, CA 92093 0820, USA
    Cell Death Differ 20:953-62. 2013
  6. pmc Colon cancer cells adopt an invasive phenotype without mesenchymal transition in 3-D but not 2-D culture upon combined stimulation with EGF and crypt growth factors
    Kirsten Ludwig
    Moores UCSD Cancer Center, 3855 Health Sciences Drive, La Jolla, CA 92093 0820, USA
    BMC Cancer 13:221. 2013
  7. doi request reprint Nuclear expression of β-catenin promotes RB stability and resistance to TNF-induced apoptosis in colon cancer cells
    Jinbo Han
    Moores UCSD Cancer Center, University of California San Diego, La Jolla, California 92093, USA
    Mol Cancer Res 11:207-18. 2013
  8. pmc Exploiting the promiscuity of imatinib
    SHUN J LEE
    Department of Medicine and Division of Hematology Oncology, 3855 Health Sciences Drive, University of California San Diego, La Jolla, CA 92093, USA
    J Biol 8:30. 2009
  9. pmc Systems analysis of quantitative shRNA-library screens identifies regulators of cell adhesion
    Xiaodong Huang
    Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093, USA
    BMC Syst Biol 2:49. 2008
  10. pmc Effect of hydroxyurea on the promoter occupancy profiles of tumor suppressor p53 and p73
    Vera Huang
    Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093 0820, USA
    BMC Biol 7:35. 2009

Collaborators

Detail Information

Publications74

  1. pmc Induction of cell retraction by the combined actions of Abl-CrkII and Rho-ROCK1 signaling
    Xiaodong Huang
    Division of Biological Sciences, Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA
    J Cell Biol 183:711-23. 2008
    ..Our results establish Rap1 as another downstream target of the Abl-CrkII signaling module and show that Abl-CrkII collaborates with Rho-ROCK1 to stimulate cell retraction...
  2. pmc Persistent inhibition of ABL tyrosine kinase causes enhanced apoptotic response to TRAIL and disrupts the pro-apoptotic effect of chloroquine
    Priya Sridevi
    Moores Cancer Center, Division of Hematology Oncology, Department of Medicine, School of Medicine, University of California San Diego, La Jolla, California, United States of America
    PLoS ONE 8:e77495. 2013
    ....
  3. pmc Separation of anti-proliferation and anti-apoptotic functions of retinoblastoma protein through targeted mutations of its A/B domain
    B Nelson Chau
    Department of Medicine, Division of Hematology Oncology, Moores UCSD Cancer Center, University of California San Diego, La Jolla, California, United States of America
    PLoS ONE 1:e82. 2006
    ..At the A/B interface is a binding site for the C-terminal trans-activation domain of E2F. Within the B-domain is a binding site for proteins containing the LxCxE peptide motif...
  4. pmc Interplay between kinase domain autophosphorylation and F-actin binding domain in regulating imatinib sensitivity and nuclear import of BCR-ABL
    Martin Preyer
    Division of Hematology Oncology and Moores Cancer Center, Department of Medicine, University of California San Diego School of Medicine, La Jolla, California, United States of America
    PLoS ONE 6:e17020. 2011
    ..The NLS function of BCR-ABL is re-activated by a kinase inhibitor, imatinib, and in a kinase-defective BCR-ABL mutant. The mechanism of this kinase-dependent inhibition of the NLS function is not understood...
  5. pmc Genetic disruption of Abl nuclear import reduces renal apoptosis in a mouse model of cisplatin-induced nephrotoxicity
    P Sridevi
    Division of Hematology Oncology, Department of Medicine, Moores UCSD Cancer Center, UCSD School of Medicine, University of California, San Diego, La Jolla, CA 92093 0820, USA
    Cell Death Differ 20:953-62. 2013
    ....
  6. pmc Colon cancer cells adopt an invasive phenotype without mesenchymal transition in 3-D but not 2-D culture upon combined stimulation with EGF and crypt growth factors
    Kirsten Ludwig
    Moores UCSD Cancer Center, 3855 Health Sciences Drive, La Jolla, CA 92093 0820, USA
    BMC Cancer 13:221. 2013
    ..Because the 3-D conditions more closely mimic the in vivo environment, we examined the effects of Wnt and other crypt growth factors on colon cancer cell growth in 3-D culture...
  7. doi request reprint Nuclear expression of β-catenin promotes RB stability and resistance to TNF-induced apoptosis in colon cancer cells
    Jinbo Han
    Moores UCSD Cancer Center, University of California San Diego, La Jolla, California 92093, USA
    Mol Cancer Res 11:207-18. 2013
    ..Together, these results suggest that nuclear β-catenin-dependent RB stabilization suppresses TNF-induced apoptosis in caspase-8-positive colon cancer cells...
  8. pmc Exploiting the promiscuity of imatinib
    SHUN J LEE
    Department of Medicine and Division of Hematology Oncology, 3855 Health Sciences Drive, University of California San Diego, La Jolla, CA 92093, USA
    J Biol 8:30. 2009
    ..A recent paper in BMC Structural Biology reports a 1.75 A crystal structure of imatinib bound to the oxidoreductase NQO2 and reveals insights into the binding specificity and the off-target effects of the inhibitor...
  9. pmc Systems analysis of quantitative shRNA-library screens identifies regulators of cell adhesion
    Xiaodong Huang
    Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093, USA
    BMC Syst Biol 2:49. 2008
    ....
  10. pmc Effect of hydroxyurea on the promoter occupancy profiles of tumor suppressor p53 and p73
    Vera Huang
    Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093 0820, USA
    BMC Biol 7:35. 2009
    ..The goal of this study was to compare the promoter-binding activity of p53 and p73 at steady state and after genotoxic stress induced by hydroxyurea...
  11. ncbi request reprint Choosing between growth arrest and apoptosis through the retinoblastoma tumour suppressor protein, Abl and p73
    J Y Wang
    Division of Biology and the Cancer Center, University of California, San Diego, La Jolla, CA 92093 0322, USA
    Biochem Soc Trans 29:666-73. 2001
    ..The antagonism between RB and c-Abl/p73 may modulate the function of p53 to direct the choice between growth arrest and apoptosis in DNA damaged cells...
  12. ncbi request reprint Nucleo-cytoplasmic communication in apoptotic response to genotoxic and inflammatory stress
    Jean Yj Wang
    Division of Biological Sciences and Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093 0322, USA
    Cell Res 15:43-8. 2005
    ..The involvement of these nuclear signal transducers in TNF induced apoptosis, which does not require new gene expression, indicates that nuclear events other than transcription can contribute to extrinsic apoptotic signal transduction...
  13. ncbi request reprint Mismatch repair proteins as sensors of alkylation DNA damage
    Jean Y J Wang
    Division of Hematology Oncology, Department of Medicine and Moores Cancer Center, University of California, San Diego, School of Medicine, 3855 Health Sciences Drive, La Jolla, California 92093, USA
    Cancer Cell 9:417-8. 2006
    ....
  14. ncbi request reprint Keystone Symposia on Molecular and Cellular Biology: 'The molecular basis of cancer'. Organizers: Carol L. Prives and George F. Vande Woude, Taos, NM, 15-21 March 1999
    J Y Wang
    Department of Biology and the Cancer Center, University of California, San Diego, La Jolla, CA 92093 0322, USA
    Biochim Biophys Acta 1470:R21-8. 2000
    ..We were unable to report on all of the talks and posters due mostly to our limited capacity to absorb and digest the large amount of results presented at the meeting. We apologize to those whose results were not covered in this report...
  15. ncbi request reprint Controlling Abl: auto-inhibition and co-inhibition?
    Jean Y J Wang
    Section of Molecular Biology, Division of Biological Sciences and the Cancer Center, University of California, San Diego, La Jolla, CA 92093 0322, USA
    Nat Cell Biol 6:3-7. 2004
    ..The implication of co-inhibition on Abl function is discussed...
  16. ncbi request reprint Role of retinoblastoma tumor suppressor protein in DNA damage response
    J Y Wang
    Division of Biology and the Cancer Center, University of California, San Diego, La Jolla, USA
    Acta Oncol 40:689-95. 2001
    ..Taken together, these results suggest that RB plays a critical role in determining the cell fate following DNA damage. Growth arrest is dependent on RB and apoptosis is activated following RB degradation...
  17. ncbi request reprint Retinoblastoma protein in growth suppression and death protection
    J Y Wang
    Department of Biology, University of California, San Diego 9500 Gilman Drive, La Jolla, California 92093 0347, USA
    Curr Opin Genet Dev 7:39-45. 1997
    ..Unbecoming of a tumor suppressor, RB has an active role in antagonizing the death response. How RB integrates its multiple functions into a tumor suppression program is still an open issue...
  18. ncbi request reprint Cellular responses to DNA damage
    J Y Wang
    Department of Biology, University of California, San Diego, La Jolla 92093 0322, USA
    Curr Opin Cell Biol 10:240-7. 1998
    ..Recently, several signaling pathways that link DNA damage to gene expression and to the cell-cycle checkpoints have been identified. These pathways establish a framework for future studies of DNA damage responses...
  19. pmc CD154 induces p73 to overcome the resistance to apoptosis of chronic lymphocytic leukemia cells lacking functional p53
    Frank Dicker
    Moores Cancer Center, University of California San Diego School of Medicine, La Jolla, CA 92093 0663, USA
    Blood 108:3450-7. 2006
    ..These results indicate that CD154 can sensitize leukemia cells to apoptosis via the c-Abl-dependent activation of p73 and mitigate the resistance of p53-deficient CLL cells to anticancer drug therapy...
  20. ncbi request reprint Differential regulation of retinoblastoma protein function by specific Cdk phosphorylation sites
    E S Knudsen
    Department of Biology, University of California at San Diego, La Jolla, California 92093 0347, USA
    J Biol Chem 271:8313-20. 1996
    ..Mutation of Ser-807/811 and Thr-821/826 does not abolish the regulation of E2F binding. Taken together, these results show that the protein binding domains of RB are each regulated by distinct Cdk phosphorylation sites...
  21. ncbi request reprint The tyrosine kinase c-Abl regulates p73 in apoptotic response to cisplatin-induced DNA damage
    J G Gong
    Department of Biology, University of California, San Diego, La Jolla 92093 0322, USA
    Nature 399:806-9. 1999
    ..Our results indicate that c-Abl and p73 are components of a mismatch-repair-dependent apoptosis pathway which contributes to cisplatin-induced cytotoxicity...
  22. pmc Establishment of irreversible growth arrest in myogenic differentiation requires the RB LXCXE-binding function
    T T Chen
    Department of Biology and the Cancer Center, University of California, San Diego, La Jolla, California 92093-0322, USA
    Mol Cell Biol 20:5571-80. 2000
    ..Moreover, the LXCXE-binding pocket is dispensable for the intrinsic growth suppression function of RB. However, the LXCXE-binding function is essential for RB to establish the serum-refractory state in differentiated myocytes...
  23. pmc Dual mechanisms for the inhibition of E2F binding to RB by cyclin-dependent kinase-mediated RB phosphorylation
    E S Knudsen
    Department of Biology and Center for Molecular Genetics, University of California at San Diego, La Jolla 92093 0322, USA
    Mol Cell Biol 17:5771-83. 1997
    ....
  24. pmc Growth suppression by an E2F-binding-defective retinoblastoma protein (RB): contribution from the RB C pocket
    L L Whitaker
    Department of Biology, Center for Molecular Genetics, and Cancer Center, University of California, San Diego, La Jolla, California 92093 0322, USA
    Mol Cell Biol 18:4032-42. 1998
    ..In addition, E2F and LXCXE binding are not the only mechanisms through which RB inhibits cell growth. The C pocket also contributes to RB-mediated growth suppression...
  25. ncbi request reprint Ataxia telangiectasia mutant protein activates c-Abl tyrosine kinase in response to ionizing radiation
    R Baskaran
    Department of Biology and Center for Molecular Genetics, University of California at San Diego, La Jolla 92093 0322, USA
    Nature 387:516-9. 1997
    ..These findings identify the c-Abl tyrosine kinase as a downstream target of phosphorylation and activation by the ATM kinase in the cellular response to ionizing radiation...
  26. ncbi request reprint The large subunit of replication factor C promotes cell survival after DNA damage in an LxCxE motif- and Rb-dependent manner
    V Pennaneach
    Sidney Kimmel Cancer Center, 10835 Altman Road, San Diego, CA 92121, USA
    Mol Cell 7:715-27. 2001
    ..The inability of wild-type RF-Cp145 to promote cell survival in Rb-null cells is rescued by Rb but not by Rb mutants defective in binding LxCxE proteins. RF-C thus enhances cell survival after DNA damage in an Rb-dependent manner...
  27. pmc Induction of JNK and c-Abl signalling by cisplatin and oxaliplatin in mismatch repair-proficient and -deficient cells
    A Nehme
    Department of Medicine and the Cancer Center, University of California, San Diego, La Jolla 92093 0058, USA
    Br J Cancer 79:1104-10. 1999
    ..In contrast, this detector does not respond to oxaliplatin adducts...
  28. pmc Global control of cell-cycle transcription by coupled CDK and network oscillators
    David A Orlando
    Department of Biology, Duke University, Durham, North Carolina 27708, USA
    Nature 453:944-7. 2008
    ..We propose that periodic transcription is an emergent property of a transcription factor network that can function as a cell-cycle oscillator independently of, and in tandem with, the CDK oscillator...
  29. ncbi request reprint A C-terminal protein-binding domain in the retinoblastoma protein regulates nuclear c-Abl tyrosine kinase in the cell cycle
    P J Welch
    Department of Biology, University of California, San Diego, La Jolla 92093 0116
    Cell 75:779-90. 1993
    ..The nuclear c-Abl tyrosine kinase can enhance transcription, and this activity is inhibited by RB. Nuclear c-Abl is an S phase-activated tyrosine kinase that may participate directly in the regulation of transcription...
  30. ncbi request reprint Three distinct signalling responses by murine fibroblasts to genotoxic stress
    Z G Liu
    Department of Pharmacology, Program in Biomedical Science, School of Medicine, University of California, San Diego 92093, USA
    Nature 384:273-6. 1996
    ..These findings show that signals generated by genotoxins are transduced by multiple, independent pathways. Only p53 appears to be a universal sensor of genotoxic stress...
  31. ncbi request reprint Class I histone deacetylases sequentially interact with MyoD and pRb during skeletal myogenesis
    P L Puri
    Department of Biology, University of California San Diego, La Jolla, CA 92093, USA
    Mol Cell 8:885-97. 2001
    ..These results suggest that reduced expression of HDAC1 accompanied by its redistribution in alternative nuclear protein complexes is critical for terminal differentiation of skeletal muscle cells...
  32. pmc Abrogation of retinoblastoma protein function by c-Abl through tyrosine kinase-dependent and -independent mechanisms
    P J Welch
    Department of Biology, University of California, San Diego, La Jolla 92093 0347, USA
    Mol Cell Biol 15:5542-51. 1995
    ..Exclusive engagement of RB by one of its many targets is incompatible with the biological function of this growth suppressor protein...
  33. doi request reprint Cell identity mediates the response of Arabidopsis roots to abiotic stress
    JOSE R DINNENY
    Department of Biology, Duke University, Durham, NC 27708, USA
    Science 320:942-5. 2008
    ..By performing a similar analysis using iron deprivation, we identified common cell-type-specific stress responses and revealed the crucial role the environment plays in defining the transcriptional outcome of cell-fate decisions...
  34. ncbi request reprint c-Abl tyrosine kinase binds and phosphorylates phospholipid scramblase 1
    J Sun
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA
    J Biol Chem 276:28984-90. 2001
    ..These findings indicate that c-Abl binds and phosphorylates PLSCR1, and raise the possibility that an interaction between c-Abl and plasma membrane PLSCR1 might contribute to the cellular response to genotoxic stress...
  35. pmc p38 and extracellular signal-regulated kinases regulate the myogenic program at multiple steps
    Z Wu
    Laboratory of Gene Regulation and Signal Transduction, University of California, San Diego, La Jolla, California 92093 0322, USA
    Mol Cell Biol 20:3951-64. 2000
    ..Importantly, activation of ERK is inhibitory toward myogenic transcription in myoblasts but contributes to the activation of myogenic transcription and regulates postmitotic responses (i.e., hypertrophic growth) in myotubes...
  36. ncbi request reprint Differential phosphorylation of c-Abl in cell cycle determined by cdc2 kinase and phosphatase activity
    E T Kipreos
    Department of Biology, University of California, San Diego, La Jolla 92093
    Science 248:217-20. 1990
    ..Treatment of interphase cells with okadaic acid leads to a rounded morphology similar to that observed during mitosis...
  37. pmc Nuclear-cytoplasmic shuttling of C-ABL tyrosine kinase
    S Taagepera
    Department of Biology, Center for Molecular Genetics and the Cancer Center, University of California at San Diego, La Jolla CA 92093 0322, USA
    Proc Natl Acad Sci U S A 95:7457-62. 1998
    ..Taken together, these results demonstrate that c-Abl shuttles continuously between the nucleus and the cytoplasm and that the rate of nuclear import and export can be modulated by the adherence status of fibroblastic cells...
  38. pmc Oncogenic v-Abl tyrosine kinase can inhibit or stimulate growth, depending on the cell context
    M W Renshaw
    Department of Biology, University of California, San Diego, La Jolla 92093 0116
    EMBO J 11:3941-51. 1992
    ..These results show that v-Abl tyrosine kinase is not an obligatory activator of growth, but requires a permissive cellular context to manifest its mitogenic function...
  39. pmc Identification of a binding site in c-Ab1 tyrosine kinase for the C-terminal repeated domain of RNA polymerase II
    R Baskaran
    Department of Biology and Center for Molecular Genetics, University of California, San Diego, La Jolla, California 93093 0347, USA
    Mol Cell Biol 16:3361-9. 1996
    ..Taken together, these observations demonstrate that c-Abl can function as a CTD kinase in vitro as well as in vivo...
  40. pmc Src homology 2 domain as a specificity determinant in the c-Abl-mediated tyrosine phosphorylation of the RNA polymerase II carboxyl-terminal repeated domain
    J Duyster
    Department of Biology, University of California, San Diego, La Jolla 92093 0347
    Proc Natl Acad Sci U S A 92:1555-9. 1995
    ..These results demonstrate that the SH2 domain of the Abl tyrosine kinase plays an active role in catalysis and suggests that SH2 domain and the tyrosine kinase domain may act in concert to confer substrate specificity...
  41. ncbi request reprint Reversible dependence on growth factor interleukin-3 in myeloid cells expressing temperature sensitive v-abl oncogene
    E T Kipreos
    Department of Biology, University of California, San Diego, La Jolla 92093
    Oncogene Res 2:277-84. 1988
    ..These results demonstrate that the maintenance of A-MuLV induced IL-3 independence requires the continuous function of the v-abl oncogene...
  42. ncbi request reprint The N-terminal region of neuregulin isoforms determines the accumulation of cell surface and released neuregulin ectodomain
    J Y Wang
    Department of Biology, Emory University, Atlanta, Georgia 30322, USA
    J Biol Chem 276:2841-51. 2001
    ....
  43. ncbi request reprint Induction of apoptosis in chronic myelogenous leukemia cells through nuclear entrapment of BCR-ABL tyrosine kinase
    P Vigneri
    Department of Biology, University of California at San Diego, La Jolla, California, USA
    Nat Med 7:228-34. 2001
    ..These results indicate that nuclear entrapment of BCR-ABL can be used as a therapeutic strategy to selectively kill chronic myelogenous leukemia cells...
  44. ncbi request reprint Reversible tyrosine phosphorylation of cdc2: dephosphorylation accompanies activation during entry into mitosis
    A O Morla
    Department of Biology, University of California, La Jolla, San Diego 92093
    Cell 58:193-203. 1989
    ..Tyrosine dephosphorylation of cdc2 may be one of a number of obligatory steps in the mitotic activation of the kinase...
  45. ncbi request reprint Inhibition of c-Abl tyrosine kinase activity by filamentous actin
    P J Woodring
    Salk Institute, La Jolla, California 92037 1099, USA
    J Biol Chem 276:27104-10. 2001
    ..Taken together, the data suggest that F-actin is an inhibitor of the c-Abl tyrosine kinase and that this inhibition contributes in part to the reduced Abl kinase activity in detached cells...
  46. ncbi request reprint Transmembrane neuregulins interact with LIM kinase 1, a cytoplasmic protein kinase implicated in development of visuospatial cognition
    J Y Wang
    Department of Biology, Emory University, Atlanta, Georgia 30322, USA
    J Biol Chem 273:20525-34. 1998
    ..To our knowledge, LIMK1 is the first identified protein shown to interact with the cytoplasmic tail of a receptor tyrosine kinase ligand...
  47. pmc c-Abl phosphorylates Dok1 to promote filopodia during cell spreading
    Pamela J Woodring
    Molecular and Cell Biology Laboratory, The Salk Institute for Biological Sciences, 10010 North Torrey Pines Rd, La Jolla, CA 92037 1099, USA
    J Cell Biol 165:493-503. 2004
    ..Our data suggest a novel pathway by which c-Abl transduces signals to the actin cytoskeleton through phosphorylating Dok1 Y361 and recruiting Nck...
  48. ncbi request reprint Exclusion of c-Abl from the nucleus restrains the p73 tumor suppression function
    Veronica Vella
    Division of Biological Sciences and the Cancer Center, University of California, San Diego, La Jolla 92093 0322, USA
    J Biol Chem 278:25151-7. 2003
    ..These results suggest subcellular segregation of c-Abl from p73 to be a strategy for disrupting the tumor suppression function of p73alpha...
  49. pmc Apoptotic function of human PMS2 compromised by the nonsynonymous single-nucleotide polymorphic variant R20Q
    Ivana Marinovic-Terzic
    Moores Cancer Center, University of California, San Diego, School of Medicine, 3855 Health Sciences Drive, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 105:13993-8. 2008
    ..Because PMS2(R20Q) lacks proapoptotic activity, this polymorphic allele may modulate tumor responses to cisplatin among cancer patients...
  50. ncbi request reprint A myogenic differentiation checkpoint activated by genotoxic stress
    Pier Lorenzo Puri
    Dulbecco Telethon Institute at Laboratory of Gene Expression, Fondazione Andrea Cesalpino University of Rome La Sapienza, 00161 Rome, Italy
    Nat Genet 32:585-93. 2002
    ..These results support the idea that genotoxic stress can regulate differentiation, and identify a new biological function for DNA damage-activated signaling network...
  51. ncbi request reprint Radiation dose-dependent maintenance of G(2) arrest requires retinoblastoma protein
    Soheil Naderi
    Department of Medical Biochemistry, University of Oslo, P O Box 1112 Blindern, Oslo N 0317, Norway
    Cell Cycle 1:193-200. 2002
    ..Thus, regulation of the RB function may be an important aspect in the maintenance of cell cycle checkpoints in DNA damage response...
  52. ncbi request reprint Coordination of repair, checkpoint, and cell death responses to DNA damage
    Jean Y J Wang
    Division of Biological Sciences and the Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093 USA
    Adv Protein Chem 69:101-35. 2004
  53. ncbi request reprint Selective Chk1 inhibitors differentially sensitize p53-deficient cancer cells to cancer therapeutics
    Zehan Chen
    Cancer Research, Abbott Laboratories, Abbott Park, IL 60064 6101, USA
    Int J Cancer 119:2784-94. 2006
    ..These results indicate that it is feasible to achieve a therapeutic window with 1 or more Chk1 inhibitors in potentiation of cancer therapy based on the status of the p53 pathway in a wide spectrum of tumor types...
  54. pmc Interaction of mismatch repair protein PMS2 and the p53-related transcription factor p73 in apoptosis response to cisplatin
    Hideki Shimodaira
    Ludwig Institute for Cancer Research, University of California at San Diego, Bonner Hall 3326, 9500 Gilman Drive, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 100:2420-5. 2003
    ..Moreover, stimulation of the p73 proapoptotic function by cisplatin requires PMS2. These results suggest that PMS2 contributes to genome integrity not only through DNA repair but also by enhancing DNA damage-induced apoptosis...
  55. pmc Ascorbate up-regulates MLH1 (Mut L homologue-1) and p73: implications for the cellular response to DNA damage
    M Valeria Catani
    Biochemistry Laboratory, IDI IRCCS, c o Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, Via Tor Vergata 135, 00133 Rome, Italy
    Biochem J 364:441-7. 2002
    ..These data suggest a potential mechanism accounting for the anti-carcinogenic and anti-cancer activities of vitamin C...
  56. ncbi request reprint Ectopic expression of p73alpha, but not p73beta, suppresses myogenic differentiation
    Chun Ying Li
    Division of Biological Sciences and Moores Cancer Center, University of California, San Diego, La Jolla, California 92093 0322, USA
    J Biol Chem 280:2159-64. 2005
    ..These results demonstrated a functional diversity between the two C-terminal variants of p73 and suggested that p73alpha can regulate cellular differentiation in addition to its role in stimulating cell death...
  57. pmc Tumor necrosis factor alpha-induced apoptosis requires p73 and c-ABL activation downstream of RB degradation
    B Nelson Chau
    Division of Biological Sciences and Cancer Center, University of California, San Diego, La Jolla, California 92093 0322, USA
    Mol Cell Biol 24:4438-47. 2004
    ..Thus, c-ABL and p73 contribute to apoptosis induced by TNF-alpha, in addition to their role in promoting DNA damage-associated cell death...
  58. ncbi request reprint Mitotic phosphorylation rescues Abl from F-actin-mediated inhibition
    Pamela J Woodring
    Molecular and Cell Biology Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037 1099, USA
    J Biol Chem 280:10318-25. 2005
    ..These results suggest that F-actin may reinforce the autoinhibitory interactions to regulate Abl kinase and that inhibition can be relieved through phosphorylation and/or protein interactions with the Abl PRL region...
  59. pmc cAMP-mediated inhibition of DNA replication and S phase progression: involvement of Rb, p21Cip1, and PCNA
    Soheil Naderi
    Institute of Basic Medical Sciences, Department of Biochemistry, University of Oslo, Oslo N 0317, Norway
    Mol Biol Cell 16:1527-42. 2005
    ..Taken together, these results demonstrate a novel role for cAMP in regulation of DNA synthesis and support a model in which activation of cAMP-dependent signaling protects cells from the effect of S phase-specific antitumor agents...
  60. ncbi request reprint Death by Abl: a matter of location
    Jiangyu Zhu
    Section of Molecular Biology, Division of Biological Sciences, University of California, San Diego, La Jolla, California 92093, USA
    Curr Top Dev Biol 59:165-92. 2004
  61. ncbi request reprint Modulation of human checkpoint kinase Chk1 by the regulatory beta-subunit of protein kinase CK2
    Barbara Guerra
    Division of Biological Sciences 0322, University of California, San Diego, CA 92093 0322, USA
    Oncogene 22:4933-42. 2003
    ..Collectively, these studies confirm the implication of the regulatory beta-subunit of protein kinase CK2 in cell cycle regulation and identify a novel mechanism for the activation of Chk1 protein kinase...
  62. pmc Modulation of DNA damage-induced apoptosis by cell adhesion is independently mediated by p53 and c-Abl
    Tony Truong
    Department of Cell Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 100:10281-6. 2003
    ..These data suggest that killing of p53-negative tumor cells by chemotherapy would be enhanced by integrin ligation to activate the alternative c-Abl/p73 pathway...
  63. ncbi request reprint Signal-dependent protection from apoptosis in mice expressing caspase-resistant Rb
    B Nelson Chau
    Division of Biology and the Cancer Center, 9500 Gilman Drive 0322, University of California, San Diego, La Jolla, California 92093 0322, USA
    Nat Cell Biol 4:757-65. 2002
    ..Our results highlight the importance of Rb cleavage in TNFRI-induced apoptosis...
  64. ncbi request reprint Reduced focal adhesion kinase and paxillin phosphorylation in BCR-ABL-transfected cells
    Keding Cheng
    Department of Bioimmunotherapy, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA
    Cancer 95:440-50. 2002
    ..The authors therefore investigated the effect of p210(BCR-ABL) on actin polymerization as well as on the expression and phosphorylation state of the adhesion proteins paxillin and focal adhesion kinase (FAK)...
  65. ncbi request reprint Coordinated regulation of life and death by RB
    B Nelson Chau
    Division of Biological Sciences and the Cancer Center, University of California, San Diego, La Jolla, California 92093 0322, USA
    Nat Rev Cancer 3:130-8. 2003
    ..Drawing from the different mechanisms of RB inactivation, we propose two models for ways in which cells use RB to make the choice of life versus death...
  66. pmc Tumor promotion by caspase-resistant retinoblastoma protein
    Helena L Borges
    Division of Hematology Oncology, Moores Cancer Center, School of Medicine, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 102:15587-92. 2005
    ..These results suggest that RB tumor suppressor function, i.e., inhibition of proliferation, is inactivated by phosphorylation, whereas RB tumor promoting function, i.e., inhibition of apoptosis, is inactivated by caspase cleavage...
  67. pmc Modulation of the F-actin cytoskeleton by c-Abl tyrosine kinase in cell spreading and neurite extension
    Pamela J Woodring
    The Salk Institute, La Jolla, CA 92037 1099, USA
    J Cell Biol 156:879-92. 2002
    ..The reciprocal regulation between F-actin and the c-Abl tyrosine kinase may provide a self-limiting mechanism in the control of actin cytoskeleton dynamics...
  68. ncbi request reprint Eph tumour suppression: the dark side of Gleevec
    Jean Y J Wang
    Nat Cell Biol 8:785-6. 2006
  69. ncbi request reprint Regulation of F-actin-dependent processes by the Abl family of tyrosine kinases
    Pamela J Woodring
    The Salk Institute, 10010 North Torrey Pines Road, La Jolla, CA 92037 1099, USA
    J Cell Sci 116:2613-26. 2003
    ..The modular structure and the nuclear-cytoplasmic shuttling of c-Abl suggest that it integrates multiple signals to coordinate F-actin dynamics with the cellular decision to differentiate or to die...
  70. ncbi request reprint Blockade of tumor necrosis factor-induced Bid cleavage by caspase-resistant Rb
    Xiaodong Huang
    Division of Biological Sciences, Department of Medicine, University of California, San Diego, La Jolla, California 92093 0820, USA
    J Biol Chem 282:29401-13. 2007
    ..These results suggest that Rb cleavage is required for Bid cleavage in TNF-induced type-2 apoptosis, and this requirement can be supplanted by the inhibition of V-ATPase...
  71. pmc Abl tyrosine kinase promotes dorsal ruffles but restrains lamellipodia extension during cell spreading on fibronectin
    Hua Jin
    Division of Biological Sciences, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093 0820, USA
    Mol Biol Cell 18:4143-54. 2007
    ..The Abl-dependent dorsal membrane localization of activated Rac explains its positive role in ruffling and negative role in cell spreading and migration...
  72. pmc DNA damage-induced cell death: lessons from the central nervous system
    Helena Lobo Borges
    Division of Hematology Oncology, Moores Cancer Center, Department of Medicine, University of California, San Diego, 3855 Health Sciences, La Jolla, CA 92093 0820, USA
    Cell Res 18:17-26. 2008
    ....
  73. pmc Selection of mammalian cells based on their cell-cycle phase using dielectrophoresis
    Unyoung Kim
    Departments of Mechanical Engineering, University of California, Santa Barbara, CA 93106, USA
    Proc Natl Acad Sci U S A 104:20708-12. 2007
    ..This work illustrates the feasibility of using laminar flow and electrokinetic forces for the efficient, noninvasive separation of living cells...
  74. pmc Acetylation of mouse p53 at lysine 317 negatively regulates p53 apoptotic activities after DNA damage
    Connie Chao
    Section of Molecular Biology, Division of Biological Sciences, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093 0322, USA
    Mol Cell Biol 26:6859-69. 2006
    ..These findings demonstrate that acetylation at lysine 317 negatively regulates p53 apoptotic activities after DNA damage...

Research Grants37

  1. CELLULAR FUNCTION OF RETINOBLASTOMA GENE PRODUCT
    Jean Wang; Fiscal Year: 1992
  2. Nuclear Function of Abl in DNA Damage Response
    Jean Wang; Fiscal Year: 2009
    ....
  3. CELLULAR FUNCTION OF THE RETINOBLASTOMA GENE PRODUCT
    Jean Wang; Fiscal Year: 2000
    ..3.To determine the role of RB in protecting cells from death by using RB mutants. ..
  4. BIOLOGICAL Function of the Retinoblastoma Gene Product
    Jean Wang; Fiscal Year: 2004
    ..These genetics programs are likely to be affected during tumor development. Therefore, the proposed research will result in the identification of important targets for therapeutic intervention in cancer treatment. ..
  5. Nuclear Function of Abl in DNA Damage Response
    Jean Y J Wang; Fiscal Year: 2010
    ....
  6. BIOLOGICAL Function of the Retinoblastoma Gene Product
    Jean Wang; Fiscal Year: 2003
    ..These genetics programs are likely to be affected during tumor development. Therefore, the proposed research will result in the identification of important targets for therapeutic intervention in cancer treatment. ..
  7. Nuclear Function of Abl in DNA Damage Response
    Jean Wang; Fiscal Year: 2009
    ..Results from this study will advance our understanding of cellular response to DNA damage and this knowledge will help to reduce the harmful side effects while improving the efficacy of cancer therapy. ..
  8. Protein Tyrosine Kinases in Leiomyomata Uteri
    Jean Wang; Fiscal Year: 2003
    ..Information gathered from the proposed research may therefore lead to the development of new therapeutics to control the growth of fibroids. ..
  9. BIOLOGICAL Function of the Retinoblastoma Gene Product
    Jean Wang; Fiscal Year: 2005
    ..These genetics programs are likely to be affected during tumor development. Therefore, the proposed research will result in the identification of important targets for therapeutic intervention in cancer treatment. ..
  10. Protein Tyrosine Kinases in Leiomyomata Uteri
    Jean Wang; Fiscal Year: 2006
    ..Information gathered from the proposed research may therefore lead to the development of new therapeutics to control the growth of fibroids. ..
  11. Nuclear Function of the c-Abl Protooncoprotien
    Jean Wang; Fiscal Year: 2007
    ..Aim 6 will implement two strategies to identify other nuclear substrates of c-Abl. Identification of substrates will provide further information on the biological function of the c-Abl tyrosine kinase. ..
  12. BIOLOGICAL Function of the Retinoblastoma Gene Product
    Jean Wang; Fiscal Year: 2002
    ..These genetics programs are likely to be affected during tumor development. Therefore, the proposed research will result in the identification of important targets for therapeutic intervention in cancer treatment. ..
  13. CELLULAR FUNCTION OF THE RETINOBLASTOMA GENE PRODUCT
    Jean Wang; Fiscal Year: 1999
    ..3.To determine the role of RB in protecting cells from death by using RB mutants. ..
  14. STRUCTURE AND FUNCTION OF C-ABL PROTO-ONCOGENE
    Jean Wang; Fiscal Year: 1992
    ..The proposed research will investigate the role of subcellular location on the regulation of the c-abl tyrosine kinase and may shed light on the pathogenic mechanism induced by an deregulated tyrosine kinase...
  15. CELLULAR FUNCTION OF THE RETINOBLASTOMA GENE PRODUCT
    Jean Wang; Fiscal Year: 2001
    ..3.To determine the role of RB in protecting cells from death by using RB mutants. ..
  16. BIOLOGICAL Function of the Retinoblastoma Gene Product
    Jean Wang; Fiscal Year: 2009
    ..Results from the proposed research will facilitate the development of new strategies to reduce the risk of inflammation-associated cancer. ..
  17. BIOLOGICAL Function of the Retinoblastoma Gene Product
    Jean Y J Wang; Fiscal Year: 2010
    ..Results from the proposed research will facilitate the development of new strategies to reduce the risk of inflammation-associated cancer. ..
  18. BIOLOGICAL Function of the Retinoblastoma Gene Product
    Jean Wang; Fiscal Year: 2007
    ..Results from the proposed research will facilitate the development of new strategies to reduce the risk of inflammation-associated cancer. ..
  19. Protein Tyrosine Kinases in Leiomyomata Uteri
    Jean Wang; Fiscal Year: 2007
    ..Information gathered from the proposed research may therefore lead to the development of new therapeutics to control the growth of fibroids. ..
  20. BIOLOGICAL Function of the Retinoblastoma Gene Product
    Jean Wang; Fiscal Year: 2006
    ..These genetics programs are likely to be affected during tumor development. Therefore, the proposed research will result in the identification of important targets for therapeutic intervention in cancer treatment. ..
  21. Protein Tyrosine Kinases in Leiomyomata Uteri
    Jean Wang; Fiscal Year: 2005
    ..Information gathered from the proposed research may therefore lead to the development of new therapeutics to control the growth of fibroids. ..
  22. Protein Tyrosine Kinases in Leiomyomata Uteri
    Jean Wang; Fiscal Year: 2004
    ..Information gathered from the proposed research may therefore lead to the development of new therapeutics to control the growth of fibroids. ..
  23. STRUCTURE AND FUNCTION OF C-ABL PROTO-ONCOGENE
    Jean Wang; Fiscal Year: 1991
    ..The proposed research will investigate the role of subcellular location on the regulation of the c-abl tyrosine kinase and may shed light on the pathogenic mechanism induced by an deregulated tyrosine kinase...
  24. CELLULAR FUNCTION OF RETINOBLASTOMA GENE PRODUCT
    Jean Wang; Fiscal Year: 1993