Michele Pagano

Summary

Affiliation: New York University
Country: USA

Publications

  1. ncbi request reprint When protein destruction runs amok, malignancy is on the loose
    Michele Pagano
    Department of Pathology and NYU Cancer Institute, MSB 599, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
    Cancer Cell 4:251-6. 2003
  2. ncbi request reprint Cell cycle, proteolysis and cancer
    Lili Yamasaki
    Biological Sciences, Columbia University, New York, USA
    Curr Opin Cell Biol 16:623-8. 2004
  3. pmc Cell Division, a new open access online forum for and from the cell cycle community
    Philipp Kaldis
    National Cancer Institute, Mouse Cancer Genetics Program, Bldg, 560 22 56, 1050 Boyles Street, Frederick, MD 21702 1201, USA
    Cell Div 1:1. 2006
  4. ncbi request reprint Wagging the dogma; tissue-specific cell cycle control in the mouse embryo
    Michele Pagano
    Department of Pathology and NYU Cancer Institute, New York University School of Medicine, New York, NY 10016, USA
    Cell 118:535-8. 2004
  5. pmc Modification of Cul1 regulates its association with proteasomal subunits
    Joanna Bloom
    Department of Pathology, New York University Cancer Institute and New York University School of Medicine, New York 10016, USA
    Cell Div 1:5. 2006
  6. pmc The Cdc14B-Cdh1-Plk1 axis controls the G2 DNA-damage-response checkpoint
    Florian Bassermann
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, NY 10016, USA
    Cell 134:256-67. 2008
  7. pmc Control of chromosome stability by the beta-TrCP-REST-Mad2 axis
    Daniele Guardavaccaro
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, New York 10016, USA
    Nature 452:365-9. 2008
  8. pmc Regulation of the CRL4(Cdt2) ubiquitin ligase and cell-cycle exit by the SCF(Fbxo11) ubiquitin ligase
    Mario Rossi
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, NY 10016, USA
    Mol Cell 49:1159-66. 2013
  9. pmc FBXL2- and PTPL1-mediated degradation of p110-free p85β regulatory subunit controls the PI(3)K signalling cascade
    Shafi Kuchay
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, New York 10016, USA
    Nat Cell Biol 15:472-80. 2013
  10. pmc Phosphorylation of Ser72 is dispensable for Skp2 assembly into an active SCF ubiquitin ligase and its subcellular localization
    Tarig Bashir
    Department of Pathology, New York University Cancer Institute, Smilow Research Center, New York University School of Medicine, New York, NY, USA
    Cell Cycle 9:971-4. 2010

Collaborators

Detail Information

Publications89

  1. ncbi request reprint When protein destruction runs amok, malignancy is on the loose
    Michele Pagano
    Department of Pathology and NYU Cancer Institute, MSB 599, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
    Cancer Cell 4:251-6. 2003
    ..Here we review the aberrant activity of a variety of ubiquitin ligases in human cancer, hence the prospect of targeting them in cancer therapy...
  2. ncbi request reprint Cell cycle, proteolysis and cancer
    Lili Yamasaki
    Biological Sciences, Columbia University, New York, USA
    Curr Opin Cell Biol 16:623-8. 2004
    ..CDKs, E2F and ubiquitin ligases reciprocally regulate each other, resulting in complex feedback loops. Perturbation of this network of molecular machines is associated with proliferative diseases, including cancer...
  3. pmc Cell Division, a new open access online forum for and from the cell cycle community
    Philipp Kaldis
    National Cancer Institute, Mouse Cancer Genetics Program, Bldg, 560 22 56, 1050 Boyles Street, Frederick, MD 21702 1201, USA
    Cell Div 1:1. 2006
    ..A major goal of this new journal is to publish timely and significant studies on the aberrations of the cell cycle network that occur in cancer and other diseases...
  4. ncbi request reprint Wagging the dogma; tissue-specific cell cycle control in the mouse embryo
    Michele Pagano
    Department of Pathology and NYU Cancer Institute, New York University School of Medicine, New York, NY 10016, USA
    Cell 118:535-8. 2004
    ....
  5. pmc Modification of Cul1 regulates its association with proteasomal subunits
    Joanna Bloom
    Department of Pathology, New York University Cancer Institute and New York University School of Medicine, New York 10016, USA
    Cell Div 1:5. 2006
    ..CONCLUSION : The association of ubiquitylating enzymes with proteasomes may be an additional means to target ubiquitylated substrates for degradation...
  6. pmc The Cdc14B-Cdh1-Plk1 axis controls the G2 DNA-damage-response checkpoint
    Florian Bassermann
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, NY 10016, USA
    Cell 134:256-67. 2008
    ..These findings define a novel pathway that is crucial for the G2 DNA-damage-response checkpoint...
  7. pmc Control of chromosome stability by the beta-TrCP-REST-Mad2 axis
    Daniele Guardavaccaro
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, New York 10016, USA
    Nature 452:365-9. 2008
    ..The high levels of REST or its truncated variants found in certain human tumours may contribute to cellular transformation by promoting genomic instability...
  8. pmc Regulation of the CRL4(Cdt2) ubiquitin ligase and cell-cycle exit by the SCF(Fbxo11) ubiquitin ligase
    Mario Rossi
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, NY 10016, USA
    Mol Cell 49:1159-66. 2013
    ..Finally, our results show that the functional interaction between FBXO11 and CDT2 is evolutionary conserved from worms to humans and plays an important role in regulating the timing of cell-cycle exit...
  9. pmc FBXL2- and PTPL1-mediated degradation of p110-free p85β regulatory subunit controls the PI(3)K signalling cascade
    Shafi Kuchay
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, New York 10016, USA
    Nat Cell Biol 15:472-80. 2013
    ..We propose that FBXL2 and PTPL1 suppress p85β levels, preventing the inhibition of PI(3)K by an excess of free p85 that could compete with p85-p110 heterodimers for IRS1...
  10. pmc Phosphorylation of Ser72 is dispensable for Skp2 assembly into an active SCF ubiquitin ligase and its subcellular localization
    Tarig Bashir
    Department of Pathology, New York University Cancer Institute, Smilow Research Center, New York University School of Medicine, New York, NY, USA
    Cell Cycle 9:971-4. 2010
    ....
  11. pmc Cyclin F-mediated degradation of ribonucleotide reductase M2 controls genome integrity and DNA repair
    Vincenzo D'Angiolella
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, NY 10016, USA
    Cell 149:1023-34. 2012
    ..In summary, we have identified a biochemical pathway that controls the abundance of dNTPs and ensures efficient DNA repair in response to genotoxic stress...
  12. pmc APC/C- and Mad2-mediated degradation of Cdc20 during spindle checkpoint activation
    Sheng Ge
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
    Cell Cycle 8:167-71. 2009
    ..We propose that the degradation of Cdc20 represents a critical control mechanism to ensure inactivation of APC/C(Cdc20) in response to the SAC...
  13. pmc SCF(Cyclin F) controls centrosome homeostasis and mitotic fidelity through CP110 degradation
    Vincenzo D'Angiolella
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, New York 10016, USA
    Nature 466:138-42. 2010
    ..We propose that SCF(Cyclin F)-mediated degradation of CP110 is required for the fidelity of mitosis and genome integrity...
  14. pmc Fbxw7α- and GSK3-mediated degradation of p100 is a pro-survival mechanism in multiple myeloma
    Luca Busino
    NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, New York 10016, USA
    Nat Cell Biol 14:375-85. 2012
    ..Thus, in multiple myeloma, Fbxw7α and GSK3 function as pro-survival factors through the control of p100 degradation...
  15. ncbi request reprint SCFbetaTrCP-mediated degradation of Claspin regulates recovery from the DNA replication checkpoint response
    Angelo Peschiaroli
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, MSB 599, New York, New York 10016, USA
    Mol Cell 23:319-29. 2006
    ..Importantly, in response to DNA damage in G2, Claspin proteolysis is inhibited to allow the prompt reestablishment of the checkpoint...
  16. pmc FBH1 promotes DNA double-strand breakage and apoptosis in response to DNA replication stress
    Yeon Tae Jeong
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, New York, NY 10016, USA
    J Cell Biol 200:141-9. 2013
    ..Our findings show that FBH1 helicase activity is required for the efficient induction of DSBs and apoptosis specifically in response to DNA replication stress...
  17. ncbi request reprint SCFFbxl3 controls the oscillation of the circadian clock by directing the degradation of cryptochrome proteins
    Luca Busino
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, NY 10016, USA
    Science 316:900-4. 2007
    ..Silencing of Fbxl3 produced no effect in Cry1-/-;Cry2-/- cells, which shows that Fbxl3 controls clock oscillations by mediating the degradation of CRY proteins...
  18. pmc APC/C(Cdc20) controls the ubiquitin-mediated degradation of p21 in prometaphase
    Virginia Amador
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue MSB 599, New York, NY 10016, USA
    Mol Cell 27:462-73. 2007
    ..We propose that the APC/C(Cdc20)-mediated degradation of p21 contributes to the full activation of Cdk1 necessary for mitotic events and prevents mitotic slippage during spindle checkpoint activation...
  19. ncbi request reprint S6K1- and betaTRCP-mediated degradation of PDCD4 promotes protein translation and cell growth
    N Valerio Dorrello
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, NY 10016, USA
    Science 314:467-71. 2006
    ..We propose that regulated degradation of PDCD4 in response to mitogens allows efficient protein synthesis and consequently cell growth...
  20. pmc USP33 regulates centrosome biogenesis via deubiquitination of the centriolar protein CP110
    Ji Li
    Department of Pathology and Cancer Institute, Smilow Research Center, New York University School of Medicine, 522 1st Avenue, New York, New York 10016, USA
    Nature 495:255-9. 2013
    ..Our results point towards potential therapeutic strategies for inhibiting tumorigenesis associated with centrosome amplification...
  21. ncbi request reprint Control of the SCF(Skp2-Cks1) ubiquitin ligase by the APC/C(Cdh1) ubiquitin ligase
    Tarig Bashir
    Department of Pathology, MSB 599, New York University School of Medicine, and New York University Cancer Institute, 550 First Avenue, New York, New York 10016, USA
    Nature 428:190-3. 2004
    ..Thus, the induction of Skp2 and Cks1 degradation in G1 represents a principal mechanism by which APC/C(Cdh1) prevents the unscheduled degradation of SCF(Skp2-Cks1) substrates and maintains the G1 state...
  22. pmc Deregulated proteolysis by the F-box proteins SKP2 and beta-TrCP: tipping the scales of cancer
    David Frescas
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA
    Nat Rev Cancer 8:438-49. 2008
    ....
  23. ncbi request reprint Structural basis of the Cks1-dependent recognition of p27(Kip1) by the SCF(Skp2) ubiquitin ligase
    Bing Hao
    Howard Hughes Medical Institute, New York, New York 10021, USA
    Mol Cell 20:9-19. 2005
    ..The structure and biochemical data support the proposed model that Cdk2-cyclin A contributes to the recruitment of p27(Kip1) to the SCF(Skp2)-Cks1 complex...
  24. ncbi request reprint JHDM1B/FBXL10 is a nucleolar protein that represses transcription of ribosomal RNA genes
    David Frescas
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA
    Nature 450:309-13. 2007
    ....
  25. pmc FBXO11 targets BCL6 for degradation and is inactivated in diffuse large B-cell lymphomas
    Shanshan Duan
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, New York, New York 10016, USA
    Nature 481:90-3. 2012
    ..The deletions/mutations found in DLBCLs are largely monoallelic, indicating that FBXO11 is a haplo-insufficient tumour suppressor gene...
  26. ncbi request reprint Involvement of the SCF complex in the control of Cdh1 degradation in S-phase
    Ramla Benmaamar
    Department of Pathology, New York University School of Medicine, New York, New York, USA
    Cell Cycle 4:1230-2. 2005
    ..Herein, we show that the SCF complex (Skp1/Cul1/F-box protein/Roc1) intervenes in the surveillance of Cdh1 cellular abundance in S-phase...
  27. pmc betaTrCP- and Rsk1/2-mediated degradation of BimEL inhibits apoptosis
    Elinor Dehan
    Department of Pathology, NYU Cancer Institute, Smilow Research Center, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
    Mol Cell 33:109-16. 2009
    ..Our findings reveal that betaTrCP promotes cell survival in cooperation with the ERK-RSK pathway by targeting BimEL for degradation...
  28. pmc KDM2A represses transcription of centromeric satellite repeats and maintains the heterochromatic state
    David Frescas
    Department of Pathology, New York University Cancer Institute, New York University School of Medicine, New York, New York 10016, USA
    Cell Cycle 7:3539-47. 2008
    ..Since the disruption of epigenetic control mechanisms contributes to cellular transformation, these results, together with the low levels of KDM2A found in prostate carcinomas, suggest a role for KDM2A in cancer development...
  29. pmc Tumor suppressor function of androgen receptor coactivator ARA70alpha in prostate cancer
    Martin Ligr
    Department of Pathology and Urology, New York University School of Medicine, New York Harbor Healthcare System, New York, NY 10010, USA
    Am J Pathol 176:1891-900. 2010
    ..Although growth inhibition by ARA70alpha is AR-dependent, the inhibition of cell invasion is an androgen-independent process. These results strongly suggest that ARA70alpha functions as a tumor suppressor gene...
  30. pmc FBH1 protects melanocytes from transformation and is deregulated in melanomas
    Yeon Tae Jeong
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, New York, NY, USA
    Cell Cycle 12:1128-32. 2013
    ..Thus, FBH1 inactivation appears to contribute to oncogenic transformation by allowing survival of cells undergoing replicative stress due to external factors such as UV irradiation...
  31. pmc Specific small molecule inhibitors of Skp2-mediated p27 degradation
    Lily Wu
    Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY 10016, USA
    Chem Biol 19:1515-24. 2012
    ..Designing SCF-Skp2-specific inhibitors may be a novel strategy to treat cancers dependent on the Skp2-p27 axis...
  32. pmc mTOR generates an auto-amplification loop by triggering the βTrCP- and CK1α-dependent degradation of DEPTOR
    Shanshan Duan
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, New York, NY 10016, USA
    Mol Cell 44:317-24. 2011
    ..Moreover, our results suggest that pharmacologic inhibition of CK1 may be a viable therapeutic option for the treatment of cancers characterized by activation of mTOR-signaling pathways...
  33. pmc Thrombin induces tumor cell cycle activation and spontaneous growth by down-regulation of p27Kip1, in association with the up-regulation of Skp2 and MiR-222
    Liang Hu
    Department of Medicine, New York University School of Medicine, New York, USA
    Cancer Res 69:3374-81. 2009
    ..04). Repetitive hirudin, a specific potent antithrombin, decreased tumor volume 13- to 24-fold (P < 0.04). Thus, thrombin stimulates tumor cell growth in vivo by down-regulation of p27(Kip1)...
  34. ncbi request reprint Degradation of Id2 by the anaphase-promoting complex couples cell cycle exit and axonal growth
    Anna Lasorella
    Institute for Cancer Genetics, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    Nature 442:471-4. 2006
    ..These findings indicate that deregulated Id activity might be useful to reprogramme quiescent neurons into the axonal growth mode...
  35. pmc The HECT-domain ubiquitin ligase Huwe1 controls neural differentiation and proliferation by destabilizing the N-Myc oncoprotein
    Xudong Zhao
    Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA
    Nat Cell Biol 10:643-53. 2008
    ..These findings indicate that Huwe1 links destruction of N-Myc to the quiescent state that complements differentiation in the neural tissue...
  36. pmc A cyclin without cyclin-dependent kinases: cyclin F controls genome stability through ubiquitin-mediated proteolysis
    Vincenzo D'Angiolella
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, New York, NY 10016, USA
    Trends Cell Biol 23:135-40. 2013
    ..We highlight the relevance of cyclin F in controlling genome stability through ubiquitin-mediated proteolysis and the implications for cancer development...
  37. pmc SCF-mediated degradation of p100 (NF-κB2): mechanisms and relevance in multiple myeloma
    Luca Busino
    NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, NY 10016, USA
    Sci Signal 5:pt14. 2012
    ..Thus, the FBXW7α-dependent degradation of p100 functions as a prosurvival mechanism through control of NF-κB activity...
  38. pmc Control of cell growth by the SCF and APC/C ubiquitin ligases
    Jeffrey R Skaar
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, New York, NY 10016, USA
    Curr Opin Cell Biol 21:816-24. 2009
    ..Our expanding understanding of the roles of the SCF and APC/C complexes highlight the potential for targeted molecular therapies...
  39. ncbi request reprint To be or not to be ubiquitinated?
    Joanna Bloom
    Department of Pathology and NYU Cancer Institute, New York University School of Medicine, New York, New York 10016, USA
    Cell Cycle 3:138-40. 2004
    ..We discuss that, with the only notable exception of ornithine decarboxylase, ubiquitination appears to be a prerequisite for proteasomal degradation rather than an unnecessary byproduct of such proteolysis...
  40. ncbi request reprint Proteasome-mediated degradation of p21 via N-terminal ubiquitinylation
    Joanna Bloom
    New York University Cancer Institute and New York University School of Medicine, New York, NY 10016, USA
    Cell 115:71-82. 2003
    ..These results demonstrate that proteasomal degradation of p21 is regulated by the ubiquitin pathway and suggest that the site of the ubiquitin chain is critical in making p21 a competent substrate for the proteasome...
  41. pmc Role of F-box protein betaTrcp1 in mammary gland development and tumorigenesis
    Yasusei Kudo
    Department of Pathology and NYU Cancer Institute, New York University School of Medicine, NY 10016, USA
    Mol Cell Biol 24:8184-94. 2004
    ....
  42. ncbi request reprint Control of DNA synthesis and mitosis by the Skp2-p27-Cdk1/2 axis
    Michele Pagano
    Department of Pathology, New York University School of Medicine and NYU Cancer Institute, 550 First Avenue, MSB 599, New York, NY 10016, USA
    Mol Cell 14:414-6. 2004
    ....
  43. pmc Cdh1: a master G0/G1 regulator
    Jeffrey R Skaar
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, NY 10016, USA
    Nat Cell Biol 10:755-7. 2008
    ..Using a conditional knockout of the Cdh1 coding gene Fizzy-related (Fzr), a new study demonstrates that Cdh1 is essential for viability and that it functions as a tumour suppressor by preventing genomic instability...
  44. pmc Stimulation of prostate cancer cellular proliferation and invasion by the androgen receptor co-activator ARA70
    Yi Peng
    Department of Pathology, New York University School of Medicine, New York Harbor Healthcare System, 423 E 23rd St, Room 6140N, New York, NY 10010, USA
    Am J Pathol 172:225-35. 2008
    ..Our findings implicate ARA70 beta as a regulator of tumor cell growth and metastasis by affecting gene expression...
  45. pmc INTS3 controls the hSSB1-mediated DNA damage response
    Jeffrey R Skaar
    Howard Hughes Medical Institute, New York University Cancer Institute, New York University School of Medicine, New York, NY 10016, USA
    J Cell Biol 187:25-32. 2009
    ..These effects on the DNA damage response are caused by the control of hSSB1 transcription via INTS3, demonstrating a new network controlling hSSB1 function...
  46. ncbi request reprint A peptidomimetic siRNA transfection reagent for highly effective gene silencing
    Yeliz Utku
    Department of Chemistry, New York University, New York, NY 10003, USA
    Mol Biosyst 2:312-7. 2006
    ..We compare the lipitoid reagent to a standard commercial transfection reagent. The lipitoid is highly efficient even in primary IMR-90 human lung fibroblasts in which other commercial reagents are typically ineffective...
  47. pmc APC/CCdh1-dependent proteolysis of USP1 regulates the response to UV-mediated DNA damage
    Xiomaris M Cotto-Rios
    Department of Biochemistry, New York University School of Medicine, New York, NY 10016, USA
    J Cell Biol 194:177-86. 2011
    ..Thus, we propose a role for APC/C(Cdh1) in modulating the status of PCNA monoubiquitination and UV DNA repair before S phase entry...
  48. ncbi request reprint Deregulated degradation of the cdk inhibitor p27 and malignant transformation
    Joanna Bloom
    Department of Pathology and NYU Cancer Instutute, MSB599, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
    Semin Cancer Biol 13:41-7. 2003
    ..More recent evidence suggests that Skp2, the specific recognition factor for p27 ubiquitination, has oncogenic properties. This review will focus on the regulation of p27 proteolysis and its consequences for tumorigenesis...
  49. ncbi request reprint Don't skip the G1 phase: how APC/CCdh1 keeps SCFSKP2 in check
    Tarig Bashir
    New York University School of Medicine, New York University Cancer Institute, New York, New York 10016, USA
    Cell Cycle 3:850-2. 2004
    ..Thus, APC/C(Cdh1), a ubiquitin ligase involved in mitotic exit and maintenance of G(0)/G(1) phase, directly controls SCF(Skp2), a ubiquitin ligase involved in the regulation of S phase entry...
  50. pmc BubR1 is modified by sumoylation during mitotic progression
    Feikun Yang
    Departments of Environmental Medicine and Pharmacology, New York University School of Medicine, Tuxedo, New York 10987, USA
    J Biol Chem 287:4875-82. 2012
    ..Combined, our study identifies a new type of post-translational modification that is essential for BubR1 function during mitosis...
  51. pmc Loss of p27KIP1 expression in fully-staged node-negative breast cancer: association with lack of hormone receptors in T1a/b, but not T1c infiltrative ductal carcinoma
    Deepu Mirchandani
    New York University School of Medicine and NYU Cancer Institute, New York, NY, USA
    Anticancer Res 31:4401-5. 2011
    ..We examined by IHC the association between nuclear p27(KIP1) expression and hormone receptor status in T1N0M0 breast cancer...
  52. ncbi request reprint Skp2, the FoxO1 hunter
    Elinor Dehan
    Department of Pathology and NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, New York 10016, USA
    Cancer Cell 7:209-10. 2005
    ..Since FoxO proteins possess tumor suppressor functions, this new finding suggests a new mechanism by which Skp2 may favor tumorigenesis...
  53. ncbi request reprint Oncogenic aberrations of cullin-dependent ubiquitin ligases
    Daniele Guardavaccaro
    Department of Pathology and NYU Cancer Institute, MSB 599, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
    Oncogene 23:2037-49. 2004
    ..In this review, we describe the role of CDLs in the ubiquitinylation of cancer-related substrates and discuss how altered ubiquitinylation by CDLs may contribute to tumor development...
  54. ncbi request reprint Butyrolactone: more than a kinase inhibitor?
    Joanna Bloom
    Department of Pathology and NYU Cancer Center MSB599, New York University School of Medicine 550 First Avenue New York, New York 10016, USA
    Cell Cycle 1:117-8. 2002
  55. pmc Wrenches in the works: drug discovery targeting the SCF ubiquitin ligase and APC/C complexes
    Timothy Cardozo
    Department of Pharmacology NYU Cancer Institute, New York University School of Medicine, 550 First Avenue MSB 599, New York, NY 10016, USA
    BMC Biochem 8:S9. 2007
    ..Publication history: Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com)...
  56. ncbi request reprint Aberrant ubiquitin-mediated proteolysis of cell cycle regulatory proteins and oncogenesis
    Tarig Bashir
    Department of Pathology and NYU Cancer Institute, New York University School of Medicine, New York, New York 10016, USA
    Adv Cancer Res 88:101-44. 2003
    ..This chapter aims to review the involvement of the ubiquitin pathway in the scheduled destruction of some important cell cycle regulators and to discuss the implications of their aberrant degradation for the development of cancer...
  57. ncbi request reprint Stabilizers and destabilizers controlling cell cycle oscillators
    Daniele Guardavaccaro
    Department of Pathology, NYU Cancer Institute, New York University School of Medicine, New York, New York 10016, USA
    Mol Cell 22:1-4. 2006
    ..The recent findings of hierarchical and connected waves of cyclin stabilizers highlight the complexity of this network...
  58. pmc Clinical relevance of SKP2 alterations in metastatic melanoma
    Amy E Rose
    Ronald O Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USA
    Pigment Cell Melanoma Res 24:197-206. 2011
    ..Copy number gain is a major contributing mechanism of SKP2 overexpression in metastatic melanoma. Results may have implications for the development of therapeutics that target SKP2...
  59. ncbi request reprint Experimental tests to definitively determine ubiquitylation of a substrate
    Joanna Bloom
    Department of Pathology, New York University School of Medicine and NYU Cancer Institute, New York, USA
    Methods Enzymol 399:249-66. 2005
    ....
  60. ncbi request reprint Control of meiotic and mitotic progression by the F box protein beta-Trcp1 in vivo
    Daniele Guardavaccaro
    Department of Pathology and New York University Cancer Institute, New York University School of Medicine, New York, NY 10016, USA
    Dev Cell 4:799-812. 2003
    ..Thus, beta-Trcp1 regulates the timely order of meiotic and mitotic events...
  61. ncbi request reprint Altered expression of p27 and Skp2 proteins in prostate cancer of African-American patients
    Marija Drobnjak
    Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Clin Cancer Res 9:2613-9. 2003
    ..The abundance of p27, an inhibitor of cell proliferation, is controlled by Skp2-dependent proteolysis...
  62. ncbi request reprint Multisite phosphorylation of nuclear interaction partner of ALK (NIPA) at G2/M involves cyclin B1/Cdk1
    Florian Bassermann
    Department of Internal Medicine III, Technical University of Munich, 81675 Munich, Germany, and Department of Pathology, St Jude Chidren s Research Hospital, Memphis, TN 38105, USA
    J Biol Chem 282:15965-72. 2007
    ..Thus, cyclin B1/Cdk1 may contribute to the regulation of its own abundance in early mitosis...
  63. pmc SCF ubiquitin ligases in the maintenance of genome stability
    Joshua S Silverman
    Department of Radiation Oncology, New York University School of Medicine, 522 First Avenue, Smilow Research Building 1107, New York, NY 10016, USA
    Trends Biochem Sci 37:66-73. 2012
    ..Given that general proteasome inhibitors are currently used as anticancer agents, a better understanding of the ubiquitylation of specific targets by specific ubiquitin ligases may result in improved cancer therapeutics...
  64. pmc Ubiquitin-dependent degradation of p73 is inhibited by PML
    Francesca Bernassola
    Molecular Biology Program, Memorial Sloan Kettering Cancer Center, 1275 York Ave, New York, NY 10021, USA
    J Exp Med 199:1545-57. 2004
    ..Our findings demonstrate that PML plays a crucial role in modulating p73 function, thus providing further insights on the molecular network for tumor suppression...
  65. ncbi request reprint The SCF ubiquitin ligase: insights into a molecular machine
    Timothy Cardozo
    Department of Pathology and New York University Cancer Institute, New York University Medical Center, 550 First Avenue, MSB 599, New York, New York 10016, USA
    Nat Rev Mol Cell Biol 5:739-51. 2004
    ..Here we explore a unifying and structurally detailed view of SCF-mediated proteolytic control of cellular processes that has been revealed by recent studies...
  66. pmc Rac1 accumulates in the nucleus during the G2 phase of the cell cycle and promotes cell division
    David Michaelson
    Department of Medicine, New York University School of Medicine, New York, NY 10016, USA
    J Cell Biol 181:485-96. 2008
    ..These results show that Rac1 cycles in and out of the nucleus during the cell cycle and thereby plays a role in promoting cell division...
  67. pmc In vivo interference with Skp1 function leads to genetic instability and neoplastic transformation
    Roberto Piva
    Department of Pathology and NYU Cancer Institute Division of Hematopathology, New York University School of Medicine, New York, New York 10016, USA
    Mol Cell Biol 22:8375-87. 2002
    ..Our findings support a crucial role for Skp1 in proper chromosomal segregation, which is required for the maintenance of euploidy and suppression of transformation...
  68. pmc S-phase kinase-associated protein 2 expression in non-Hodgkin's lymphoma inversely correlates with p27 expression and defines cells in S phase
    Roberto Chiarle
    Department of Pathology and Kaplan Comprehensive CancerCenter, New York University School of Medicine, New York, New York
    Am J Pathol 160:1457-66. 2002
    ..The detection of Skp2 protein either by flow cytometry or by immunohistochemistry represents a simple method to precisely assess the S phase of lymphomas. The potential diagnostic and prognostic value of Skp2 is discussed...
  69. ncbi request reprint Degradation of Cdc25A by beta-TrCP during S phase and in response to DNA damage
    Luca Busino
    European Institute of Oncology, 435 Via Ripamonti, 20141 Milan, Italy
    Nature 426:87-91. 2003
    ..Our results show that beta-TrCP has a crucial role in mediating the response to DNA damage through Cdc25A degradation...
  70. ncbi request reprint Substrate recognition and ubiquitination of SCFSkp2/Cks1 ubiquitin-protein isopeptide ligase
    Shuichan Xu
    Department of Biochemistry and Biomarker Development, Signal Pharmaceuticals, LLC, San Diego, California 92121, USA
    J Biol Chem 282:15462-70. 2007
    ..In the absence of p27, Cdk2/E and Cks1 increase Skp2 phosphorylation. This phosphorylation enhances Skp2 auto-ubiquitination, whereas p27 inhibits both phosphorylation and auto-ubiquitination of Skp2...
  71. ncbi request reprint The acidic tail domain of human Cdc34 is required for p27Kip1 ubiquitination and complementation of a cdc34 temperature sensitive yeast strain
    Karen Block
    Department of Medicine, Division of Nephrology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229, USA
    Cell Cycle 4:1421-7. 2005
    ....
  72. ncbi request reprint Skp2 contains a novel cyclin A binding domain that directly protects cyclin A from inhibition by p27Kip1
    Peng Ji
    Department of Developmental and Molecular Biology, the Albert Einstein Comprehensive Cancer Center and Liver Research Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Biol Chem 281:24058-69. 2006
    ..These findings reveal a new functional mechanism of Skp2 and a new regulatory mechanism of cyclin A...
  73. pmc Dual mode of degradation of Cdc25 A phosphatase
    Maddalena Donzelli
    European Institute of Oncology, 435 Via Ripamonti, I 20141 Milan, Italy
    EMBO J 21:4875-84. 2002
    ..We propose that a dual mechanism of regulated degradation allows for fine tuning of Cdc25 A abundance in response to cell environment...
  74. ncbi request reprint Three different binding sites of Cks1 are required for p27-ubiquitin ligation
    Danielle Sitry
    Unit of Biochemistry, The B Rappaport Faculty of Medicine, Technion Israel Institute of Technology, Haifa 31096, Israel
    J Biol Chem 277:42233-40. 2002
    ..The interaction of Skp2 with the substrate is further strengthened by the association of the Cdk-binding site of Cks1 with Cdk2/cyclin E, to which phosphorylated p27 is bound...
  75. ncbi request reprint Structure of the Cul1-Rbx1-Skp1-F boxSkp2 SCF ubiquitin ligase complex
    Ning Zheng
    Cellular Biochemistry and Biophysics Program, Memorial Sloan Kettering Cancer Center, New York 10021, USA
    Nature 416:703-9. 2002
    ..The structure suggests that Cul1 may contribute to catalysis through the positioning of the substrate and the ubiquitin-conjugating enzyme, and this model is supported by Cul1 mutations designed to eliminate the rigidity of the scaffold...
  76. ncbi request reprint The after-hours mutant reveals a role for Fbxl3 in determining mammalian circadian period
    Sofia I H Godinho
    Medical Research Council MRC Mammalian Genetics Unit, Harwell, Oxfordshire OX11 0RD, UK
    Science 316:897-900. 2007
    ..The Afh allele significantly affected Per2 expression and delayed the rate of Cry protein degradation in Per2::Luciferase tissue slices. Our in vivo and in vitro studies reveal a central role for Fbxl3 in mammalian circadian timekeeping...
  77. pmc Constitutive phosphorylation of aurora-a on ser51 induces its stabilization and consequent overexpression in cancer
    Shojiro Kitajima
    Department of Oral and Maxillofacial Pathobiology, Division of Frontier Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan
    PLoS ONE 2:e944. 2007
    ..Here we tested the hypothesis that aberration of the protein destruction system induces accumulation and consequently overexpression of Aur-A in cancer...
  78. ncbi request reprint DRE-1: an evolutionarily conserved F box protein that regulates C. elegans developmental age
    Nicole Fielenbach
    Baylor College of Medicine, Huffington Center on Aging, Department of Molecular and Cellular Biology, One Baylor Plaza, Houston, TX 77030, USA
    Dev Cell 12:443-55. 2007
    ..The identification of core components involved in SCF-mediated modification and/or proteolysis suggests an important level of regulation in the heterochronic hierarchy...
  79. ncbi request reprint Cdk1: the dominant sibling of Cdk2
    Tarig Bashir
    Nat Cell Biol 7:779-81. 2005
  80. ncbi request reprint Alterations in the expression of the cell cycle regulatory protein cyclin kinase subunit 1 in colorectal carcinoma
    Ma anit Shapira
    Department of Surgery A, Rambam Medical Center, Technion Israel Institute of Technology, Haifa, Israel
    Cancer 100:1615-21. 2004
    ..The essential role of cyclin kinase subunit 1 (Cks1) in Skp2-dependent p27 degradation was recently discovered, but its role in human malignancies is unknown...
  81. ncbi request reprint Varshavsky's contributions
    Wolfgang Baumeister
    Science 306:1290-2. 2004
  82. pmc Novel p27(kip1) C-terminal scatter domain mediates Rac-dependent cell migration independent of cell cycle arrest functions
    Sandra S McAllister
    Howard Hughes Medical Institute, University of California San Diego School of Medicine, La Jolla 92093 0686, USA
    Mol Cell Biol 23:216-28. 2003
    ..These observations define a novel role for p27 in cell motility that is independent of its function in cell cycle inhibition...
  83. ncbi request reprint Role of the SCFSkp2 ubiquitin ligase in the degradation of p21Cip1 in S phase
    Gil Bornstein
    Unit of Biochemistry, The B Rappaport Faculty of Medicine, Technion Israel Institute of Technology, Haifa 31096, Israel
    J Biol Chem 278:25752-7. 2003
    ..It is suggested that SCFSkp2 participates in the degradation of p21 in the S phase...
  84. ncbi request reprint An Rb-Skp2-p27 pathway mediates acute cell cycle inhibition by Rb and is retained in a partial-penetrance Rb mutant
    Peng Ji
    Department of Developmental and Molecular Biology, The Albert Einstein Comprehensive Cancer Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Mol Cell 16:47-58. 2004
    ..These results identify an Rb-Skp2-p27 pathway in Rb function, which may be involved in inhibition of tumor progression...
  85. pmc Role of Polo-like kinase in the degradation of early mitotic inhibitor 1, a regulator of the anaphase promoting complex/cyclosome
    Yakir Moshe
    Unit of Biochemistry, The Bruce Rappaport Faculty of Medicine, Technion Israel Institute of Technology, Haifa 31096, Israel
    Proc Natl Acad Sci U S A 101:7937-42. 2004
    ..Transfection with an small interfering RNA duplex directed against Plk1 caused the accumulation of Emi1 in mitotically arrested HeLa cells. It is suggested that phosphorylation of Emi1 by Plk1 is involved in its degradation in mitosis...
  86. pmc Oncogenic role of the ubiquitin ligase subunit Skp2 in human breast cancer
    Sabina Signoretti
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA
    J Clin Invest 110:633-41. 2002
    ..We conclude that Skp2 has oncogenic potential in breast epithelial cells and is overexpressed in a subset of breast carcinomas (ER- and Her-2 negative) for which Skp2 inhibitors may represent a valid therapeutic option...
  87. ncbi request reprint The pRb-Cdh1-p27 autoamplifying network
    Patricia G Santamaria
    Nat Cell Biol 9:137-8. 2007
  88. pmc Role of Cks1 overexpression in oral squamous cell carcinomas: cooperation with Skp2 in promoting p27 degradation
    Shojiro Kitajima
    Department of Oral Maxillofacial Pathobiology, Division of Frontier Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, Minami Ku, Hiroshima 734 8553, Japan
    Am J Pathol 165:2147-55. 2004
    ..These findings suggest that Cks1 overexpression may play an important role for OSCC development through Skp2-mediated p27 degradation, and that Cks1 siRNA can be a novel modality of gene therapy...
  89. pmc PCNA-dependent regulation of p21 ubiquitylation and degradation via the CRL4Cdt2 ubiquitin ligase complex
    Tarek Abbas
    Department of Biochemistry and Molecular Genetics, University of Virginia, School of Medicine, Charlottesville, Virginia 22908, USA
    Genes Dev 22:2496-506. 2008
    ..Finally, we show that the CRL4(Cdt2) and the SCF(Skp2) ubiquitin ligases are redundant with each other in promoting the degradation of p21 during an unperturbed S phase of the cell cycle...