K A Roth

Summary

Affiliation: Washington University School of Medicine
Country: USA

Publications

  1. pmc Epistatic and independent functions of caspase-3 and Bcl-X(L) in developmental programmed cell death
    K A Roth
    Department of Pathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 97:466-71. 2000
  2. ncbi request reprint DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3
    C D'Sa-Eipper
    Department of Pathology, Division of Neuropathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Development 128:137-46. 2001
  3. ncbi request reprint Bcl-X(L)-caspase-9 interactions in the developing nervous system: evidence for multiple death pathways
    A U Zaidi
    Department of Pathology and Immunology, Division of Neuropathology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 21:169-75. 2001
  4. ncbi request reprint Neural precursor cells possess multiple p53-dependent apoptotic pathways
    R S Akhtar
    Department of Pathology, Division of Neuropathology, University of Alabama at Birmingham, SC 961, 1530 3rd Avenue South, Birmingham, AL 35294 0017, USA
    Cell Death Differ 13:1727-39. 2006
  5. ncbi request reprint p53 deficiency fails to prevent increased programmed cell death in the Bcl-X(L)-deficient nervous system
    B J Klocke
    Department of Pathology and Immunology Division of Neuropathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Cell Death Differ 9:1063-8. 2002
  6. ncbi request reprint Bid regulation of neuronal apoptosis
    J R Leonard
    Department of Neurological Surgery, Washington University School of Medicine, 660 S Euclid Avenue Box 8118, St Louis, MO 63110, USA
    Brain Res Dev Brain Res 128:187-90. 2001
  7. ncbi request reprint Rnx deficiency results in congenital central hypoventilation
    S Shirasawa
    Howard Hughes Medical Institute, Departments of Medicine and Pathology, Washington University School of Medicine, St Louis, Missouri, USA
    Nat Genet 24:287-90. 2000
  8. ncbi request reprint Chloroquine-induced neuronal cell death is p53 and Bcl-2 family-dependent but caspase-independent
    A U Zaidi
    Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, 63110, USA
    J Neuropathol Exp Neurol 60:937-45. 2001
  9. ncbi request reprint Ethanol-induced neuronal apoptosis in vivo requires BAX in the developing mouse brain
    C Young
    Department of Psychiatry, Washington University School of Medicine, St Louis, MO 63110, USA
    Cell Death Differ 10:1148-55. 2003
  10. ncbi request reprint Neural precursor cell apoptosis and glial tumorigenesis following transplacental ethyl-nitrosourea exposure
    J R Leonard
    Department of Pathology and Immunology, Division of Neuropathology, Washington University School of Medicine, St. Louis, MO 63110, USA
    Oncogene 20:8281-6. 2001

Collaborators

Detail Information

Publications29

  1. pmc Epistatic and independent functions of caspase-3 and Bcl-X(L) in developmental programmed cell death
    K A Roth
    Department of Pathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 97:466-71. 2000
    ....
  2. ncbi request reprint DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3
    C D'Sa-Eipper
    Department of Pathology, Division of Neuropathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Development 128:137-46. 2001
    ....
  3. ncbi request reprint Bcl-X(L)-caspase-9 interactions in the developing nervous system: evidence for multiple death pathways
    A U Zaidi
    Department of Pathology and Immunology, Division of Neuropathology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 21:169-75. 2001
    ..In total, these results indicate a transition from Caspase-9- to Bax- and Bcl-X(L)-mediated neuronal apoptosis...
  4. ncbi request reprint Neural precursor cells possess multiple p53-dependent apoptotic pathways
    R S Akhtar
    Department of Pathology, Division of Neuropathology, University of Alabama at Birmingham, SC 961, 1530 3rd Avenue South, Birmingham, AL 35294 0017, USA
    Cell Death Differ 13:1727-39. 2006
    ..These findings indicate that p53 is in a unique position to regulate at least two distinct signaling portals that activate the intrinsic apoptotic death pathway in NPCs...
  5. ncbi request reprint p53 deficiency fails to prevent increased programmed cell death in the Bcl-X(L)-deficient nervous system
    B J Klocke
    Department of Pathology and Immunology Division of Neuropathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Cell Death Differ 9:1063-8. 2002
    ..These findings suggest that Bcl-X(L) expression in the developing nervous system critically regulates neuronal responsiveness to an apoptotic stimulus other than inadequate DNA repair or cell cycle abnormalities...
  6. ncbi request reprint Bid regulation of neuronal apoptosis
    J R Leonard
    Department of Neurological Surgery, Washington University School of Medicine, 660 S Euclid Avenue Box 8118, St Louis, MO 63110, USA
    Brain Res Dev Brain Res 128:187-90. 2001
    ..We conclude that bid does not play an essential role in either naturally occurring or genotoxin-induced neuronal cell death...
  7. ncbi request reprint Rnx deficiency results in congenital central hypoventilation
    S Shirasawa
    Howard Hughes Medical Institute, Departments of Medicine and Pathology, Washington University School of Medicine, St Louis, Missouri, USA
    Nat Genet 24:287-90. 2000
    ..Thus, Rnx is critical for the development of the ventral medullary respiratory centre and its deficiency results in a syndrome resembling congenital central hypoventilation...
  8. ncbi request reprint Chloroquine-induced neuronal cell death is p53 and Bcl-2 family-dependent but caspase-independent
    A U Zaidi
    Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, 63110, USA
    J Neuropathol Exp Neurol 60:937-45. 2001
    ..Caspase-9- and caspase-3-deficient neurons were not protected from chloroquine cytotoxicity. These studies indicate that chloroquine activates a regulated cell death pathway that partially overlaps with the apoptotic cascade...
  9. ncbi request reprint Ethanol-induced neuronal apoptosis in vivo requires BAX in the developing mouse brain
    C Young
    Department of Psychiatry, Washington University School of Medicine, St Louis, MO 63110, USA
    Cell Death Differ 10:1148-55. 2003
    ..Therefore, it appears that ethanol-induced neuroapoptosis is an intrinsic pathway-mediated phenomenon involving Bax-induced disruption of mitochondrial membranes and cytochrome c release as early events leading to caspase-3 activation...
  10. ncbi request reprint Neural precursor cell apoptosis and glial tumorigenesis following transplacental ethyl-nitrosourea exposure
    J R Leonard
    Department of Pathology and Immunology, Division of Neuropathology, Washington University School of Medicine, St. Louis, MO 63110, USA
    Oncogene 20:8281-6. 2001
    ..These results suggest that intrauterine exposure of NPCs to certain DNA damaging agents may synergistically interact with specific genetic abnormalities (e.g. p53 deficiency) to produce glial neoplasms in the adult brain...
  11. ncbi request reprint Apoptosis and brain development
    K A Roth
    Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Ment Retard Dev Disabil Res Rev 7:261-6. 2001
    ..Pathological activation of apoptotic death pathways may lead to neuroanatomic abnormalities and possibly to developmental disabilities...
  12. ncbi request reprint Bax deficiency prevents the increased cell death of immature neurons in bcl-x-deficient mice
    K S Shindler
    Department of Pathology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 17:3112-9. 1997
    ..These results suggest that Bax critically interacts with Bcl-xL to regulate survival of immature neurons, but indicate that other cell death regulating proteins, in addition to Bcl-xL and Bax, also function during CNS development...
  13. pmc Acute neonatal glucocorticoid exposure produces selective and rapid cerebellar neural progenitor cell apoptotic death
    K K Noguchi
    Department of Psychiatry, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110 1093, USA
    Cell Death Differ 15:1582-92. 2008
    ..This vulnerability may be related to the physiological role of glucocorticoids in regulating programmed cell death in the mammalian cerebellum...
  14. ncbi request reprint Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis
    X M Yin
    Department of Pathology, Washington University School of Medicine, Howard Hughes Medical Institute, St Louis, Missouri 63110, USA
    Nature 400:886-91. 1999
    ..This loss-of-function model indicates that Bid is a critical substrate in vivo for signalling by death-receptor agonists, which mediates a mitochondrial amplification loop that is essential for the apoptosis of selected cells...
  15. ncbi request reprint Neurokinin B- and substance P-like immunoreactivity are co-localized in enteric nerves of rat ileum
    A M Yunker
    Department of Pathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Regul Pept 80:67-74. 1999
    ..These results indicate that PPT B products P2 and NKB are localized in a subpopulation of enteric nerves containing TKs encoded by PPT A. Stimulation of these nerves may release NKB to activate local neurokinin receptors...
  16. ncbi request reprint Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice
    N Motoyama
    Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, MO 63110
    Science 267:1506-10. 1995
    ..The life-span of immature lymphocytes, but not mature lymphocytes, was shortened. Thus, Bcl-x functions to support the viability of immature cells during the development of the nervous and hematopoietic systems...
  17. ncbi request reprint Differential susceptibility of prevertebral and paravertebral sympathetic ganglia to experimental injury
    R E Schmidt
    Department of Pathology, Washington University School of Medicine, Saint Louis, MO 63110
    Brain Res 460:214-26. 1988
    ..Differences in the susceptibility of sympathetic ganglia to various insults may underlie the selective and heterogeneous involvement of sympathetic ganglia in clinical and experimental situations...
  18. ncbi request reprint Effect of streptozotocin-induced diabetes on NGF, P75(NTR) and TrkA content of prevertebral and paravertebral rat sympathetic ganglia
    R E Schmidt
    Department of Pathology, Division of Neuropathology, Saint Louis, MO 63110, USA
    Brain Res 867:149-56. 2000
    ..These observations suggest that increased NGF content in sympathetic ganglia innervating the diabetic alimentary tract coupled with intact receptor expression may produce aberrant axonal sprouting and neuroaxonal dystrophy...
  19. ncbi request reprint Bcl-2 family and the central nervous system: from rheostat to real complex
    J J Shacka
    Division of Neuropathology, Department of Pathology, Birmingham, AL 35233 0017, USA
    Cell Death Differ 13:1299-304. 2006
  20. ncbi request reprint Caspases, apoptosis, and Alzheimer disease: causation, correlation, and confusion
    K A Roth
    Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA
    J Neuropathol Exp Neurol 60:829-38. 2001
    ....
  21. ncbi request reprint Enx (Hox11L1)-deficient mice develop myenteric neuronal hyperplasia and megacolon
    S Shirasawa
    Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Nat Med 3:646-50. 1997
    ..These results suggest that Enx is required for the proper positional specification and differentiative cell fate of enteric neurons...
  22. ncbi request reprint DNA microarrays and beyond: completing the journey from tissue to cell
    J C Mills
    Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Nat Cell Biol 3:E175-8. 2001
    ....
  23. ncbi request reprint Cellular immune responses are essential for the development of Helicobacter felis-associated gastric pathology
    K A Roth
    Department of Pathology, Center for Immunology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Immunol 163:1490-7. 1999
    ..felis infection. These results indicate that in addition to specific Helicobacter virulence factors, the host immune response is an important determinant of Helicobacter-associated disease...
  24. ncbi request reprint Deafferentation-induced abnormal neurofilament phosphorylation in red nucleus neurones
    R M Torack
    Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neuropathol Appl Neurobiol 27:444-50. 2001
    ..Resolution of these cytoskeletal abnormalities was accompanied by increased expression of the calcium binding protein, parvalbumin, suggesting that alterations in intraneuronal calcium levels may modify the deafferentation response...
  25. ncbi request reprint Apaf1 (CED-4 homolog) regulates programmed cell death in mammalian development
    F Cecconi
    Department of Molecular Cell Biology, Max Planck Institute of Biophysical Chemistry, Gottingen, Germany
    Cell 94:727-37. 1998
    ..elegans, this phenotype can be correlated with a defect of apoptosis. Our findings suggest that Apaf1 is essential for Casp3 activation in embryonic brain and is a key regulator of developmental programmed cell death in mammals...
  26. ncbi request reprint In situ immunodetection of activated caspase-3 in apoptotic neurons in the developing nervous system
    A Srinivasan
    Idun Pharmaceuticals, Inc, La Jolla, California 92037, USA
    Cell Death Differ 5:1004-16. 1998
    ..These studies indicate that caspase-3 is activated during apoptosis in the developing nervous system in vivo and that CM1 is a useful reagent for its in situ detection...
  27. ncbi request reprint Liver fatty acid-binding protein: a marker for studying cellular differentiation in gut epithelial neoplasms
    S L Carroll
    Department of Pathology, Washington University School of Medicine, St Louis, Missouri
    Gastroenterology 99:1727-35. 1990
    ..Liver fatty acid-binding protein is also a potentially useful diagnostic marker for colorectal and hepatic carcinomas...
  28. pmc Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death
    M C Wei
    Howard Hughes Medical Institute, Departments of Pathology and Medicine, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Science 292:727-30. 2001
    ..Thus, activation of a "multidomain" proapoptotic member, BAX or BAK, appears to be an essential gateway to mitochondrial dysfunction required for cell death in response to diverse stimuli...
  29. pmc The Min (multiple intestinal neoplasia) mutation: its effect on gut epithelial cell differentiation and interaction with a modifier system
    A R Moser
    McArdle Laboratory, University of Wisconsin, Madison 53706
    J Cell Biol 116:1517-26. 1992
    ....