J Yuan

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint A first insight into the molecular mechanisms of apoptosis
    Junying Yuan
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, Massachusetts 02115, USA
    Cell 116:S53-6, 1 p following S59. 2004
  2. ncbi request reprint Apoptosis in the nervous system
    J Yuan
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 407:802-9. 2000
  3. ncbi request reprint Distinct downstream pathways of caspase-11 in regulating apoptosis and cytokine maturation during septic shock response
    S J Kang
    Department of Cell Biology, Harvard Medical School, 240 Longwood Ave, Boston, MA 02115, USA
    Cell Death Differ 9:1115-25. 2002
  4. ncbi request reprint Caspase-2 deficiency prevents programmed germ cell death resulting from cytokine insufficiency but not meiotic defects caused by loss of ataxia telangiectasia-mutated (Atm) gene function
    Y Morita
    Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital Harvard Medical School, Boston, Massachusetts 02114, USA
    Cell Death Differ 8:614-20. 2001
  5. pmc Cross-talk between two cysteine protease families. Activation of caspase-12 by calpain in apoptosis
    T Nakagawa
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Cell Biol 150:887-94. 2000
  6. ncbi request reprint Caspase-12 compensates for lack of caspase-2 and caspase-3 in female germ cells
    Y Takai
    Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital Harvard Medical School, Boston, Massachusetts 02114, USA
    Apoptosis 12:791-800. 2007
  7. ncbi request reprint Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta
    T Nakagawa
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 403:98-103. 2000
  8. pmc Defects in regulation of apoptosis in caspase-2-deficient mice
    L Bergeron
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Genes Dev 12:1304-14. 1998
  9. pmc Caspase-dependent activation of cyclin-dependent kinases during Fas-induced apoptosis in Jurkat cells
    B B Zhou
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 95:6785-90. 1998
  10. ncbi request reprint Caspase-8 is required for cell death induced by expanded polyglutamine repeats
    I Sanchez
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Neuron 22:623-33. 1999

Collaborators

Detail Information

Publications55

  1. ncbi request reprint A first insight into the molecular mechanisms of apoptosis
    Junying Yuan
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, Massachusetts 02115, USA
    Cell 116:S53-6, 1 p following S59. 2004
  2. ncbi request reprint Apoptosis in the nervous system
    J Yuan
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 407:802-9. 2000
    ..Elucidation of the cell death machinery in neurons promises to provide multiple points of therapeutic intervention in neurodegenerative diseases...
  3. ncbi request reprint Distinct downstream pathways of caspase-11 in regulating apoptosis and cytokine maturation during septic shock response
    S J Kang
    Department of Cell Biology, Harvard Medical School, 240 Longwood Ave, Boston, MA 02115, USA
    Cell Death Differ 9:1115-25. 2002
    ..Furthermore, we show that caspase-11-mediated apoptosis under septic condition is Bid-independent. Our work suggests that the human homologue of caspase-11 may be an effective therapeutic target for treatment of septic shock...
  4. ncbi request reprint Caspase-2 deficiency prevents programmed germ cell death resulting from cytokine insufficiency but not meiotic defects caused by loss of ataxia telangiectasia-mutated (Atm) gene function
    Y Morita
    Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital Harvard Medical School, Boston, Massachusetts 02114, USA
    Cell Death Differ 8:614-20. 2001
    ..Thus, genetically distinct mechanisms exist for developmental deletion of oocytes via programmed cell death, one of which probably functions as a meiotic quality-control checkpoint that cannot be overridden...
  5. pmc Cross-talk between two cysteine protease families. Activation of caspase-12 by calpain in apoptosis
    T Nakagawa
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Cell Biol 150:887-94. 2000
    ..These data suggest a novel apoptotic pathway involving calcium-mediated calpain activation and cross-talks between calpain and caspase families...
  6. ncbi request reprint Caspase-12 compensates for lack of caspase-2 and caspase-3 in female germ cells
    Y Takai
    Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital Harvard Medical School, Boston, Massachusetts 02114, USA
    Apoptosis 12:791-800. 2007
    ..However, when DNA damage is involved, and in the absence of caspase-2 and -3, caspase-12 becomes upregulated and mediates apoptosis in oocytes...
  7. ncbi request reprint Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta
    T Nakagawa
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 403:98-103. 2000
    ..Thus, caspase-12 mediates an ER-specific apoptosis pathway and may contribute to amyloid-beta neurotoxicity...
  8. pmc Defects in regulation of apoptosis in caspase-2-deficient mice
    L Bergeron
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Genes Dev 12:1304-14. 1998
    ..Thus, caspase-2 acts both as a positive and negative cell death effector, depending upon cell lineage and stage of development...
  9. pmc Caspase-dependent activation of cyclin-dependent kinases during Fas-induced apoptosis in Jurkat cells
    B B Zhou
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 95:6785-90. 1998
    ..Our results do not support the idea that apoptosis is simply an aberrant mitosis but, instead, suggest that a subset of mitotic mechanisms plays an important role in apoptosis through elevated cdk activities...
  10. ncbi request reprint Caspase-8 is required for cell death induced by expanded polyglutamine repeats
    I Sanchez
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Neuron 22:623-33. 1999
    ..These results suggest an essential role of caspase-8 in HD-related neural degenerative diseases...
  11. ncbi request reprint Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis
    H Li
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cell 94:491-501. 1998
    ..Coexpression of BclxL inhibits all the apoptotic changes induced by tBID. Our results indicate that BID is a mediator of mitochondrial damage induced by Casp8...
  12. pmc Comparative evaluation of the antitumor activity of antiangiogenic proteins delivered by gene transfer
    C J Kuo
    Department of Genetics, Harvard Medical School, Division of Molecular Medicine, Children's Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 98:4605-10. 2001
    ....
  13. ncbi request reprint The Caenorhabditis elegans cell death gene ced-4 encodes a novel protein and is expressed during the period of extensive programmed cell death
    J Yuan
    Program in Neuroscience, Harvard Medical School, Boston, MA 02115
    Development 116:309-20. 1992
    ..The Ced-4 protein, as deduced from cDNA and genomic DNA clones, is 549 amino acids in length. Two regions of the putative Ced-4 protein product show some similarity to known calcium-binding domains...
  14. ncbi request reprint Murine caspase-11, an ICE-interacting protease, is essential for the activation of ICE
    S Wang
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cell 92:501-9. 1998
    ..Our data suggest that caspase-11 is a component of ICE complex and is required for the activation of ICE...
  15. ncbi request reprint Identification of small-molecule inhibitors of interaction between the BH3 domain and Bcl-xL
    A Degterev
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, Massachusetts 02115, USA
    Nat Cell Biol 3:173-82. 2001
    ..Our results indicate that BH3-dependent heterodimerization is the key function of anti-apoptotic Bcl-2 family members and is required for the maintenance of cellular homeostasis...
  16. ncbi request reprint Specific proteolysis of the kinase protein kinase C-related kinase 2 by caspase-3 during apoptosis. Identification by a novel, small pool expression cloning strategy
    V L Cryns
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 272:29449-53. 1997
    ..Both of the major apoptotic cleavage sites of PRK2 in vivo lie within its regulatory domain, suggesting that its activity may be deregulated by proteolysis...
  17. ncbi request reprint Essential requirement for caspase-8/FLICE in the initiation of the Fas-induced apoptotic cascade
    P Juo
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Curr Biol 8:1001-8. 1998
    ..The intracellular domain of Fas interacts with several proteins including FADD (MORT-1), DAXX, RIP, FAF-1, FAP-1 and Sentrin. The adaptor protein FADD can, in turn, interact with the cysteine protease caspase-8 (FLICE/MACH/Mch5)...
  18. ncbi request reprint Kinetics of placenta growth factor/vascular endothelial growth factor synergy in endothelial hydraulic conductivity and proliferation
    R O Dull
    Edwin L. Steele Laboratory, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, 100 Blossom Street, COX 7, Boston, Massachusetts 02114, USA
    Microvasc Res 61:203-10. 2001
    ..PlGF also potentiated the effect of VEGF on BAEC proliferation. Thus, augmentation of VEGF action by PlGF depends on the duration of PlGF exposure and on the origin of endothelial cells...
  19. ncbi request reprint Wedelolactone suppresses LPS-induced caspase-11 expression by directly inhibiting the IKK complex
    M Kobori
    Department of Cell Biology, Harvard Medical School, Boston, MA, USA
    Cell Death Differ 11:123-30. 2004
    ..We demonstrate that wedelolactone is an inhibitor of IKK, a kinase critical for activation of NF-kappaB by mediating phosphorylation and degradation of IkappaBalpha...
  20. pmc Expression of a dominant negative mutant of interleukin-1 beta converting enzyme in transgenic mice prevents neuronal cell death induced by trophic factor withdrawal and ischemic brain injury
    R M Friedlander
    Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Charlestown 02129, USA
    J Exp Med 185:933-40. 1997
    ..Our data suggest that genetic manipulation using ICE family dominant negative inhibitors can ameliorate the extent of ischemia-induced brain injury and preserve neurological function...
  21. pmc Inhibition of cell migration by PITENINs: the role of ARF6
    B Miao
    Department of Biochemistry, Tufts University School of Medicine, Boston, MA 02111, USA
    Oncogene 31:4317-32. 2012
    ..Overall, our studies demonstrate the feasibility of developing specific small-molecule targeting PIP3 binding by PH domains as potential anticancer agents that can simultaneously interfere with cancer development at multiple points...
  22. ncbi request reprint Inhibition of caspase-1 slows disease progression in a mouse model of Huntington's disease
    V O Ona
    Department of Surgery, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 399:263-7. 1999
    ..In addition, we demonstrate that intracerebroventricular administration of a caspase inhibitor delays disease progression and mortality in the mouse model of Huntington's disease...
  23. pmc The channel of death
    A Degterev
    Department of Cell Biology, Harvard Medical School, 240 Longwood Ave, Boston, MA 02115, USA
    J Cell Biol 155:695-8. 2001
    ....
  24. ncbi request reprint The Peutz-Jegher gene product LKB1 is a mediator of p53-dependent cell death
    P Karuman
    Department of Cell Biology, Harvard Medical School, 02115, Boston, MA, USA
    Mol Cell 7:1307-19. 2001
    ..We propose that a deficiency in apoptosis is a key factor in the formation of multiple benign intestinal polyps in PJS patients, and possibly for the subsequent development of malignant tumors in these patients...
  25. ncbi request reprint Processing and activation of pro-interleukin-16 by caspase-3
    Y Zhang
    Pulmonary Center, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 273:1144-9. 1998
    ..Pro-IL-16 is a substrate for caspase-3, and cleavage by this enzyme releases biologically active IL-16 from its inactive precursor...
  26. pmc Combination oral antiangiogenic therapy with thalidomide and sulindac inhibits tumour growth in rabbits
    H M Verheul
    Department of Surgery, Children s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Br J Cancer 79:114-8. 1999
    ..When given together, the growth of the V2 carcinoma was inhibited by 75%. Our results indicated that oral antiangiogenic combination therapy with thalidomide and sulindac may be a useful non-toxic treatment for cancer...
  27. doi request reprint A pharmacoproteomic approach implicates eukaryotic elongation factor 2 kinase in ER stress-induced cell death
    M Boyce
    Department of Cell Biology, Harvard Medical School, Boston, MA, USA
    Cell Death Differ 15:589-99. 2008
    ..Our work identifies eEF-2K as a new component of the ER stress response and underlines the utility of novel small molecules in discovering new cell biology...
  28. ncbi request reprint Caspases: an ancient cellular sword of Damocles
    M Boyce
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Cell Death Differ 11:29-37. 2004
    ..This review summarizes the current information on the mechanisms and functions of non-mammalian caspases and their relatives in apoptotic and nonapoptotic processes, and explores the possible evolutionary origin of the caspase family...
  29. ncbi request reprint Rapid ocular angiogenic control via naked DNA delivery to cornea
    S U Stechschulte
    The Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA
    Invest Ophthalmol Vis Sci 42:1975-9. 2001
    ..The method described is safe, effective, titratable, and easily monitored. Naked DNA delivery to the cornea has the potential to alter the treatment of a wide variety of corneal and anterior segment diseases...
  30. ncbi request reprint Activation of caspase-2 in apoptosis
    H Li
    Cardiovascular Research Center, Massachusetts General Hospital East, Charlestown, Massachusetts 02129 and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 272:21010-7. 1997
    ....
  31. ncbi request reprint Sealing one's fate: control of cell death in neurons
    L Bergeron
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Curr Opin Neurobiol 8:55-63. 1998
    ..In addition, recent evidence suggests that the components in the developmental programmed cell death pathway may play a critical role in neurodegenerative disorders...
  32. pmc A novel role for RIP1 kinase in mediating TNFα production
    D E Christofferson
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Cell Death Dis 3:e320. 2012
    ..These findings implicate cIAP1/2 and Traf2 as negative regulators of this RIP1 kinase-dependent TNFα production pathway and suggest a novel role for RIP1 kinase in mediating TNFα production under certain conditions...
  33. ncbi request reprint Cellular response to endoplasmic reticulum stress: a matter of life or death
    M Boyce
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Cell Death Differ 13:363-73. 2006
    ..Here, we review what is known about the ESR in both yeast and mammals, and highlight recent findings on the mechanism and pathophysiological importance of ER stress-induced apoptosis...
  34. ncbi request reprint Expression cloning of protein targets for 3-phosphorylated phosphoinositides
    V R Rao
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 274:37893-900. 1999
    ..This report demonstrates the utility of this technique for isolating and characterizing 3'-PPI-binding proteins and has broad applicability for the isolation of binding domains for other lipid products...
  35. pmc Lateral view flow system for studies of cell adhesion and deformation under flow conditions
    J Yuan
    Massachusetts General Hospital, Boston, MA, USA
    Biotechniques 30:388-94. 2001
    ..This novel lateral view flow system provides a powerful technique for visualizing and quantifying the morphological changes of cells in contact with substrates exposed to shear stress...
  36. doi request reprint Caspases in apoptosis and beyond
    J Li
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Oncogene 27:6194-206. 2008
    ..Such knowledge is beginning to be translated into new therapies for the treatment of human diseases...
  37. ncbi request reprint The C. elegans cell death gene ced-3 encodes a protein similar to mammalian interleukin-1 beta-converting enzyme
    J Yuan
    Program of Neurosciences, Harvard Medical School, Boston, Massachusetts 02115
    Cell 75:641-52. 1993
    ..We propose that the CED-3 protein acts as a cysteine protease in the initiation of programmed cell death in C. elegans and that cysteine proteases also function in programmed cell death in mammals...
  38. ncbi request reprint Inactivation of farnesyltransferase and geranylgeranyltransferase I by caspase-3: cleavage of the common alpha subunit during apoptosis
    K W Kim
    Department of Life Science, Kwangju Institute of Science and Technology, Puk Gu, Kwangju 500 712, Korea
    Oncogene 20:358-66. 2001
    ..Taken together, we suggest that cleavage of prenyltransferase by caspase contributes to the progression of apoptosis...
  39. ncbi request reprint Inhibition of glycogen synthase kinase 3beta suppresses coxsackievirus-induced cytopathic effect and apoptosis via stabilization of beta-catenin
    J Yuan
    Department of Pathology and Laboratory Medicine, The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, University of British Columbia St Paul s Hospital, Vancouver, British Columbia, Canada
    Cell Death Differ 12:1097-106. 2005
    ..Taken together, our results demonstrate that CVB3 infection stimulates GSK3beta activity via a tyrosine kinase-dependent mechanism, which contributes to CVB3-induced CPE and apoptosis through dysregulation of beta-catenin...
  40. ncbi request reprint Inhibition of MD-1 expression by immunosuppressants or antisense oligodeoxynucleotides on skin allograft survival in mice
    X Zhang
    Key Laboratory of Organ Transplantation, Ministry of Education, PR China
    Transplant Proc 37:1965-7. 2005
    ..The aim of this study was to investigate the effects of inhibition of MD-1 expression using nonspecific immunosuppressants and specific antisense oligodeoxynucleotides (AS-ODNs) treatment on skin allograft survival in mice...
  41. ncbi request reprint Solution structure of BID, an intracellular amplifier of apoptotic signaling
    J J Chou
    Committee on Higher Degrees in Biophysics, Harvard University, Cambridge, Massachusetts 02138, USA
    Cell 96:615-24. 1999
    ..Additionally, we show that the overall structure of BID is preserved after cleavage by Caspase 8. We propose that BID has both BH3 domain-dependent and -independent modes of action in inducing mitochondrial damage...
  42. ncbi request reprint Notch1 induces cell cycle arrest and apoptosis in human cervical cancer cells: involvement of nuclear factor kappa B inhibition
    J Yao
    Institute of Virology, School of Medicine, Wuhan University, Wuhan, Hubei, People s Republic of China
    Int J Gynecol Cancer 17:502-10. 2007
    ..Overall, our results suggest that NF-kappaB inhibition may contribute partially to cell cycle arrest and apoptosis induced by Notch1 activation in human cervical cancer cells...
  43. ncbi request reprint Adhesion induced expression of the serine/threonine kinase Fnk in human macrophages
    U Holtrich
    Department of Obstetrics and Gynecology, J W Goethe University, Frankfurt, Germany
    Oncogene 19:4832-9. 2000
    ..Moreover, both proteins were shown to co-localize in mammalian cells. The homology of Cib with calmodulin and with calcineurin B suggests that Cib might be a regulatory subunit of polo-like kinases...
  44. ncbi request reprint Ich-1, an Ice/ced-3-related gene, encodes both positive and negative regulators of programmed cell death
    L Wang
    Cardiovascular Research Center, Massachusetts General Hospital East Charlestown 02129
    Cell 78:739-50. 1994
    ..These observations suggest that Ich-1 plays an important role in both positive and negative regulation of programmed cell death in vertebrate animals...
  45. ncbi request reprint Association of transcription factor APRF and protein kinase Jak1 with the interleukin-6 signal transducer gp130
    C Lutticken
    Institute for Biochemistry, RWTH Aachen, Germany
    Science 263:89-92. 1994
    ..These data indicate that Jak family protein kinases may participate in IL-6 signaling and that APRF may be activated in a complex with gp130...
  46. pmc Caspase-11 mediates oligodendrocyte cell death and pathogenesis of autoimmune-mediated demyelination
    S Hisahara
    Division of Neuroanatomy, Department of Neuroscience, Osaka University Graduate School of Medicine, Osaka 565 0871, Japan
    J Exp Med 193:111-22. 2001
    ..Our findings suggest that OLG death is mediated by a pathway that involves caspases-11 and -3 and leads to the demyelination observed in EAE...
  47. ncbi request reprint ASH2L: alternative splicing and downregulation during induced megakaryocytic differentiation of multipotential leukemia cell lines
    J Wang
    Department of Biochemistry, Institute of Basic Medical Sciences, 5 Dong Dan San Tiao, Beijing, 100005, P R China
    J Mol Med (Berl) 79:399-405. 2001
    ..These results suggest that ASH2L plays a role in hematopoiesis and is associated with some special kinds of leukemia...
  48. ncbi request reprint Overexpression of the transmembrane tyrosine phosphatase LAR activates the caspase pathway and induces apoptosis
    L P Weng
    Pulmonary Center Department of Medicine Department of Biochemistry Boston University Medical Center Boston, Massachusetts 02118, USA
    Curr Biol 8:247-56. 1998
    ..This study investigates the potential role of LAR in the regulation of cell growth and death in mammals...
  49. ncbi request reprint Characterization of the avian Ich-1 cDNA and expression of Ich-1L mRNA in the hen ovary
    A L Johnson
    Department of Biological Sciences, The University of Notre Dame, IN 46556, USA
    Gene 192:227-33. 1997
    ..The deduced amino acid (aa) sequence of ICH-1L is 70.8% identical to human ICH-1L and contains the conserved QACRG peptide active catalytic sequence characteristic of many ICE-related family of cysteine proteases...
  50. ncbi request reprint The C. elegans MDL-1 and MXL-1 proteins can functionally substitute for vertebrate MAD and MAX
    J Yuan
    Department of Molecular Biology, Princeton University, New Jersey 08544 1014, USA
    Oncogene 17:1109-18. 1998
    ..Like the vertebrate MAD protein, MDL-1 activity in suppressing transformation is dependent on a functional SIN3 interaction domain...
  51. ncbi request reprint [An experimental study on the release of endotoxin from gram negative bacteria induced by antibiotics]
    N Xu
    Institute of Burn Research, Southwestern Hospital Third Military Medical vniversity, Chongqing 400038, P.R. China
    Zhonghua Shao Shang Za Zhi 17:75-9. 2001
    ..Antibiotics with less ability of inducing LPS release were recommended for clinical management of the sepsis and/or septic shock caused by Gram negative bacteria...
  52. ncbi request reprint [The effect of Lipopolysacharide (LPS) on morphology and function of human umbilical endothelial cells (HUVECs)]
    J Cheng
    Institute of Burn Research, Southwestern Hospital, The Third Military Medical University, Chongqing 400038 P, China
    Zhonghua Shao Shang Za Zhi 17:155-8. 2001
    ..As a result, LPS might play important roles in the increase of vascular permeability, the promotion of leukocytic adherence, and the initiation of inflammatory cascade reaction...
  53. ncbi request reprint Human ICE/CED-3 protease nomenclature
    E S Alnemri
    Cell 87:171. 1996
  54. ncbi request reprint Identification and characterization of Ich-3, a member of the interleukin-1beta converting enzyme (ICE)/Ced-3 family and an upstream regulator of ICE
    S Wang
    Cardiovascular Research Center, Massachusetts General Hospital East, Charlestown, Massachusetts 02129, USA
    J Biol Chem 271:20580-7. 1996
    ..Ich-3 does not process proIL-1beta directly but does promote proIL-1beta processing by ICE. These results suggest that Ich-3 may play a very important role in apoptosis and inflammatory responses and may be an upstream regulator of ICE...
  55. ncbi request reprint Tolerization of dendritic cells by T(S) cells: the crucial role of inhibitory receptors ILT3 and ILT4
    C C Chang
    Department of Pathology, Columbia University, New York, NY 10032, USA
    Nat Immunol 3:237-43. 2002
    ..These findings demonstrate an important mechanism of immune regulation...