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Andreas Bergmann PhD

InstitutionUMass Chan Medical School
DepartmentMolecular, Cell and Cancer Biology
AddressUMass Chan Medical School
364 Plantation Street LRB Suite 419
Worcester MA 01605
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    Other Positions
    InstitutionT.H. Chan School of Medicine
    DepartmentMolecular, Cell and Cancer Biology

    InstitutionT.H. Chan School of Medicine
    DivisionCellular Biology & Imaging

    InstitutionMorningside Graduate School of Biomedical Sciences
    DepartmentCancer Biology

    InstitutionMorningside Graduate School of Biomedical Sciences
    DepartmentMD/PhD Program

    InstitutionMorningside Graduate School of Biomedical Sciences
    DepartmentPostbaccalaureate Research Education Program

    Collapse Biography 
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    Max Planck Institute for Developmental Biology, Tubingen, , GermanyBSBiochemistry
    Universitat Tubingen, Tubingen, , GermanyPHDBiology/Genetics

    Collapse Overview 
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    Genetic Control of Programmed Cell Death (Apoptosis) in Drosophila

    The long-term objective of our research is to gain a comprehensive understanding ofAndreasBergmann thegenetic control of apoptosis and cell proliferation, and their connection to human cancer. Apoptosis and cell proliferation are critical for normal development, homeostasis and aging. Inappropriate control is associated with various diseases including cancer and neurodegeneration. We are utilizing the fruit fly Drosophila melanogaster as a genetic model organism. Knowledge obtained in our studies will provide new insights for our understanding of these diseases.

    A tutorial in the lab will provide a detailed introduction into modern Drosophila techniques with emphasis on visualizing gene activity and cell death in wild-type and various mutant backgrounds, phenotypic analysis, generating transgenic flies and small scale genetic screens. In addition, students will gain experience in basic molecular biology and protein chemistry. The experiments will be aided by state-of-the-art facilities.

    Three major projects are under study in the lab.

    1. Genetic screening

    We have developed a novel genetic screening method to identify genes involved in cell death control and execution in Drosophila (Figure 1). However, unexpectedly, we also identified genes involved in growth control, signal transduction and tumor suppression. These interesting genes and their role in normal development are currently under intensive study in the lab.

    2. Discovery of non-autonomous tumor suppressor genes

    We have discovered a novel class of tumor suppressor genes. Normally, cells that lose tumor suppressor genes by genetic inactivation become highly proliferative and resistant to apoptosis, thus promoting tumor formation. However, in our studies, we identified genes which behave differently. If these genes are mutant, it is not the mutant cells which are overgrowing. Instead, the mutant cells influence the behavior of neighboring cells and promote their proliferation and increased apoptotic resistance, causing non-autonomous overgrowth. Thus, these genes qualify as non-autonomous tumor suppressors.

    How do non-autonomous tumor suppressor genes work? One class of non-autonomous mutants affects negative regulators of the Hedgehog (Hh) pathway such as patched or PKA, causing deregulated Hh signaling. This deregulated activity promotes non-autonomous proliferation as well as increased apoptosis resistance through up-regulation of Diap1, a potent inhibitor of apoptosis (Figure 2). The non-autonomous control of proliferation and apoptosis by Hh signaling may be needed to generate a supportive micro-environment for tumorigenesis.

    3. Apoptosis-induced compensatory proliferation (CP) and its implications for cancer

    Before they die, apoptotic cells can secrete cytokines. These cytokines stimulate proliferation of neighboring cells, a process referred to as apoptosis-induced compensatory proliferation (CP). There are two distinct types of apoptosis-induced compensatory proliferation. The first one is triggered when massive apoptosis is induced in proliferation-competent tissue (Figure 3). In extreme cases, this form of CP causes overgrowth which may be relevant for cancer (Figure 4). The second type of CP occurs when apoptosis is induced in post-mitotic tissue (Figure 5).

    Understanding the molecular mechanisms of CP is important for cancer research for three reasons. First, apoptosis-induced proliferation resembles inflammation-induced cancer where inflammatory cells secrete cytokines promoting the growth of cancer cells. Second, therapeutic treatment of tumors often seeks to induce apoptosis of cancer cells. However, this may be counter-productive as apoptotic cells can induce proliferation of adjacent cells. In extreme cases, we observe overgrowth of apoptotic tissue. Third, a very important question in cancer research is how transformed cells start proliferating. This is not a trivial question. Cells in a differentiated tissue have exited the cell cycle and rest in a quiescent state. The exact molecular mechanisms by which transformed cells re-enter the cell cycle are largely unknown. The second type of CP may provide answers to this question. When we induce apoptosis in the Drosophila retina which is composed of postmitotic neurons, cone and pigment cells, the neurons produce mitogens which stimulate other cells to re-enter the cell cycle (Figure 5). The characteristics of this cell cycle re-entry are similar to mammalian cells stimulated to re-enter the cell cycle.

    Thus, these examples illustrate the importance of CP in for cancer. In genetic screens, we have identified several genes involved in CP. We are analyzing these genes to understand the mechanism of CP and their potential role in cancer.


    Initially, the primary focus of research in the laboratory centered on apoptosis. However, over the years it became clear that in the context of a multi-cellular organism such as Drosophila, apoptosis is intimately linked to cell proliferation and tumor suppression. The discovery of apoptosis-induced compensatory proliferation is an instructive example. Although the cells are dying, they are able to produce cytokines that stimulate proliferation. In extreme cases, this can cause overgrowth. Because induction of apoptosis in tumor cells is a preferred strategy in the clinic, it is important to understand the mechanism of apoptosis-induced proliferation. Likewise, tumor cells need a supportive cellular micro-environment for tumorigenesis. Non-autonomous tumor suppressor genes may generate such a supportive environment. Therefore, it is important to understand the mechanism of action of these genes. The projects in the laboratory are aimed at these questions.






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    Please contact the Human Resources at UMass for openings in Dr. Bergmann's lab.

    Collapse Bibliographic 
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    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
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    1. Suthar KP, Bergmann A. Something new under the sun: caspases promote cell survival under moderate heat stress. EMBO Rep. 2023 06 05; 24(6):e57276. PMID: 37165748.
      Citations: 1     Fields:    Translation:Animals
    2. Farrell L, Puig-Barbe A, Haque MI, Amcheslavsky A, Yu M, Bergmann A, Fan Y. Actin remodeling mediates ROS production and JNK activation to drive apoptosis-induced proliferation. PLoS Genet. 2022 12; 18(12):e1010533. PMID: 36469525.
      Citations: 1     Fields:    Translation:Animals
    3. Yarikipati P, Bergmann A. In Vitro Cleavage Assays using Purified Recombinant Drosophila Caspases for Substrate Screening. J Vis Exp. 2022 10 06; (188). PMID: 36282715.
      Citations:    Fields:    Translation:AnimalsCells
    4. Shields A, Amcheslavsky A, Brown E, Lee TV, Nie Y, Tanji T, Ip YT, Bergmann A. Toll-9 interacts with Toll-1 to mediate a feedback loop during apoptosis-induced proliferation in Drosophila. Cell Rep. 2022 05 17; 39(7):110817. PMID: 35584678.
      Citations: 3     Fields:    Translation:Animals
    5. Bergmann A. Erebosis is a new type of cell death for tissue homeostasis in the Drosophila intestine. PLoS Biol. 2022 04; 20(4):e3001614. PMID: 35472045.
      Citations: 1     Fields:    Translation:AnimalsCells
    6. Lindblad JL, Tare M, Amcheslavsky A, Shields A, Bergmann A. Non-apoptotic enteroblast-specific role of the initiator caspase Dronc for development and homeostasis of the Drosophila intestine. Sci Rep. 2021 01 29; 11(1):2645. PMID: 33514791.
      Citations: 4     Fields:    Translation:Animals
    7. Amcheslavsky A, Lindblad JL, Bergmann A. Transiently "Undead" Enterocytes Mediate Homeostatic Tissue Turnover in the Adult Drosophila Midgut. Cell Rep. 2020 11 24; 33(8):108408. PMID: 33238125.
      Citations: 9     Fields:    Translation:AnimalsCells
    8. Diwanji N, Bergmann A. Basement membrane damage by ROS- and JNK-mediated Mmp2 activation drives macrophage recruitment to overgrown tissue. Nat Commun. 2020 07 20; 11(1):3631. PMID: 32686670.
      Citations: 23     Fields:    Translation:AnimalsCells
    9. Diwanji N, Bergmann A. Two Sides of the Same Coin - Compensatory Proliferation in Regeneration and Cancer. Adv Exp Med Biol. 2019; 1167:65-85. PMID: 31520349.
      Citations: 8     Fields:    Translation:HumansAnimals
    10. Bergmann A. Are membranes non-apoptotic compartments for apoptotic caspases? Oncotarget. 2018 Aug 03; 9(60):31566-31567. PMID: 30167077.
      Citations: 4     Fields:    
    11. Amcheslavsky A, Wang S, Fogarty CE, Lindblad JL, Fan Y, Bergmann A. Plasma Membrane Localization of Apoptotic Caspases for Non-apoptotic Functions. Dev Cell. 2018 05 21; 45(4):450-464.e3. PMID: 29787709.
      Citations: 29     Fields:    Translation:AnimalsCells
    12. P?rez E, Lindblad JL, Bergmann A. Tumor-promoting function of apoptotic caspases by an amplification loop involving ROS, macrophages and JNK in Drosophila. Elife. 2017 08 30; 6. PMID: 28853394.
      Citations: 35     Fields:    Translation:AnimalsCells
    13. Diwanji N, Bergmann A. An unexpected friend - ROS in apoptosis-induced compensatory proliferation: Implications for regeneration and cancer. Semin Cell Dev Biol. 2018 08; 80:74-82. PMID: 28688927.
      Citations: 41     Fields:    Translation:HumansAnimalsCells
    14. Yenigun VB, Sirito M, Amcheslavky A, Czernuszewicz T, Colonques-Bellmunt J, Garc?a-Alcover I, Wojciechowska M, Bolduc C, Chen Z, L?pez Castel A, Krahe R, Bergmann A. (CCUG)n RNA toxicity in a Drosophila model of myotonic dystrophy type 2 (DM2) activates apoptosis. Dis Model Mech. 2017 08 01; 10(8):993-1003. PMID: 28623239.
      Citations: 6     Fields:    Translation:HumansAnimalsCells
    15. Fogarty CE, Bergmann A. Killers creating new life: caspases drive apoptosis-induced proliferation in tissue repair and disease. Cell Death Differ. 2017 08; 24(8):1390-1400. PMID: 28362431.
      Citations: 92     Fields:    Translation:HumansAnimalsCells
    16. P?rez E, Bergmann A. Intercellular cannibalism fuels tumor growth. Cell Death Differ. 2017 05; 24(5):759-760. PMID: 28338659.
      Citations: 2     Fields:    Translation:HumansAnimals
    17. Kamber Kaya HE, Ditzel M, Meier P, Bergmann A. An inhibitory mono-ubiquitylation of the Drosophila initiator caspase Dronc functions in both apoptotic and non-apoptotic pathways. PLoS Genet. 2017 02; 13(2):e1006438. PMID: 28207763.
      Citations: 24     Fields:    Translation:AnimalsCells
    18. Henssen AG, Odersky A, Szymansky A, Seiler M, Althoff K, Beckers A, Speleman F, Sch?fers S, De Preter K, Astrahanseff K, Struck J, Schramm A, Eggert A, Bergmann A, Schulte JH. Targeting tachykinin receptors in neuroblastoma. Oncotarget. 2017 Jan 03; 8(1):430-443. PMID: 27888795.
      Citations: 11     Fields:    Translation:HumansAnimalsCells
    19. Li M, Lindblad JL, Perez E, Bergmann A, Fan Y. Autophagy-independent function of Atg1 for apoptosis-induced compensatory proliferation. BMC Biol. 2016 08 19; 14:70. PMID: 27542914.
      Citations: 8     Fields:    Translation:AnimalsCells
    20. Diwanji N, Bergmann A. The beneficial role of extracellular reactive oxygen species in apoptosis-induced compensatory proliferation. Fly (Austin). 2017 01 02; 11(1):46-52. PMID: 27575697.
      Citations: 18     Fields:    Translation:Animals
    21. Orme MH, Liccardi G, Moderau N, Feltham R, Wicky-John S, Tenev T, Aram L, Wilson R, Bianchi K, Morris O, Monteiro Domingues C, Robertson D, Tare M, Wepf A, Williams D, Bergmann A, Gstaiger M, Arama E, Ribeiro PS, Meier P. The unconventional myosin CRINKLED and its mammalian orthologue MYO7A regulate caspases in their signalling roles. Nat Commun. 2016 Mar 10; 7:10972. PMID: 26960254.
      Citations: 14     Fields:    Translation:HumansAnimalsCells
    22. Fogarty CE, Diwanji N, Lindblad JL, Tare M, Amcheslavsky A, Makhijani K, Br?ckner K, Fan Y, Bergmann A. Extracellular Reactive Oxygen Species Drive Apoptosis-Induced Proliferation via Drosophila Macrophages. Curr Biol. 2016 Mar 07; 26(5):575-84. PMID: 26898463.
      Citations: 93     Fields:    Translation:AnimalsCells
    23. Fogarty CE, Bergmann A. The Sound of Silence: Signaling by Apoptotic Cells. Curr Top Dev Biol. 2015; 114:241-65. PMID: 26431570.
      Citations: 31     Fields:    Translation:HumansAnimalsCells
    24. Fan Y, Bergmann A. Multiple mechanisms modulate distinct cellular susceptibilities toward apoptosis in the developing Drosophila eye. Dev Cell. 2014 Jul 14; 30(1):48-60. PMID: 24981611.
      Citations: 25     Fields:    Translation:AnimalsCells
    25. Fan Y, Wang S, Hernandez J, Yenigun VB, Hertlein G, Fogarty CE, Lindblad JL, Bergmann A. Genetic models of apoptosis-induced proliferation decipher activation of JNK and identify a requirement of EGFR signaling for tissue regenerative responses in Drosophila. PLoS Genet. 2014 Jan; 10(1):e1004131. PMID: 24497843.
      Citations: 55     Fields:    Translation:HumansAnimalsCells
    26. Fogarty CE, Bergmann A. Detecting caspase activity in Drosophila larval imaginal discs. Methods Mol Biol. 2014; 1133:109-17. PMID: 24567098.
      Citations: 10     Fields:    Translation:HumansAnimals
    27. Woodfield SE, Graves HK, Hernandez JA, Bergmann A. De-regulation of JNK and JAK/STAT signaling in ESCRT-II mutant tissues cooperatively contributes to neoplastic tumorigenesis. PLoS One. 2013; 8(2):e56021. PMID: 23418496.
      Citations: 14     Fields:    Translation:AnimalsCells
    28. Denton D, Aung-Htut MT, Lorensuhewa N, Nicolson S, Zhu W, Mills K, Cakouros D, Bergmann A, Kumar S. UTX coordinates steroid hormone-mediated autophagy and cell death. Nat Commun. 2013; 4:2916. PMID: 24336022.
      Citations: 29     Fields:    Translation:AnimalsCells
    29. Ryoo HD, Bergmann A. The role of apoptosis-induced proliferation for regeneration and cancer. Cold Spring Harb Perspect Biol. 2012 Aug 01; 4(8):a008797. PMID: 22855725.
      Citations: 113     Fields:    Translation:HumansAnimalsCells
    30. Graves HK, Woodfield SE, Yang CC, Halder G, Bergmann A. Notch signaling activates Yorkie non-cell autonomously in Drosophila. PLoS One. 2012; 7(6):e37615. PMID: 22679484.
      Citations: 14     Fields:    Translation:AnimalsCells
    31. Christiansen AE, Ding T, Bergmann A. Ligand-independent activation of the Hedgehog pathway displays non-cell autonomous proliferation during eye development in Drosophila. Mech Dev. 2012 Jul; 129(5-8):98-108. PMID: 22677792.
      Citations: 12     Fields:    Translation:HumansAnimalsCells
    32. Lee TV, Fan Y, Wang S, Srivastava M, Broemer M, Meier P, Bergmann A. Drosophila IAP1-mediated ubiquitylation controls activation of the initiator caspase DRONC independent of protein degradation. PLoS Genet. 2011 Sep; 7(9):e1002261. PMID: 21909282.
      Citations: 32     Fields:    Translation:AnimalsCells
    33. Anderson AE, Karandikar UC, Pepple KL, Chen Z, Bergmann A, Mardon G. The enhancer of trithorax and polycomb gene Caf1/p55 is essential for cell survival and patterning in Drosophila development. Development. 2011 May; 138(10):1957-66. PMID: 21490066.
      Citations: 20     Fields:    Translation:HumansAnimalsCells
    34. Bergmann A, Steller H. Apoptosis, stem cells, and tissue regeneration. Sci Signal. 2010 Oct 26; 3(145):re8. PMID: 20978240.
      Citations: 148     Fields:    Translation:HumansAnimalsCells
    35. Wang Y, Chen Z, Bergmann A. Regulation of EGFR and Notch signaling by distinct isoforms of D-cbl during Drosophila development. Dev Biol. 2010 Jun 01; 342(1):1-10. PMID: 20302857.
      Citations: 13     Fields:    Translation:AnimalsCells
    36. Herz HM, Madden LD, Chen Z, Bolduc C, Buff E, Gupta R, Davuluri R, Shilatifard A, Hariharan IK, Bergmann A. The H3K27me3 demethylase dUTX is a suppressor of Notch- and Rb-dependent tumors in Drosophila. Mol Cell Biol. 2010 May; 30(10):2485-97. PMID: 20212086.
      Citations: 67     Fields:    Translation:HumansAnimalsCells
    37. Bergmann A. The role of ubiquitylation for the control of cell death in Drosophila. Cell Death Differ. 2010 Jan; 17(1):61-7. PMID: 19498442.
      Citations: 25     Fields:    Translation:AnimalsCells
    38. Fan Y, Bergmann A. The cleaved-Caspase-3 antibody is a marker of Caspase-9-like DRONC activity in Drosophila. Cell Death Differ. 2010 Mar; 17(3):534-9. PMID: 19960024.
      Citations: 93     Fields:    Translation:HumansAnimalsCells
    39. Fan Y, Lee TV, Xu D, Chen Z, Lamblin AF, Steller H, Bergmann A. Dual roles of Drosophila p53 in cell death and cell differentiation. Cell Death Differ. 2010 Jun; 17(6):912-21. PMID: 19960025.
      Citations: 42     Fields:    Translation:HumansAnimals
    40. Allton K, Jain AK, Herz HM, Tsai WW, Jung SY, Qin J, Bergmann A, Johnson RL, Barton MC. Trim24 targets endogenous p53 for degradation. Proc Natl Acad Sci U S A. 2009 Jul 14; 106(28):11612-6. PMID: 19556538.
      Citations: 145     Fields:    Translation:HumansAnimalsCells
    41. Herz HM, Bergmann A. Genetic analysis of ESCRT function in Drosophila: a tumour model for human Tsg101. Biochem Soc Trans. 2009 Feb; 37(Pt 1):204-7. PMID: 19143632.
      Citations: 10     Fields:    Translation:HumansAnimalsCells
    42. Herz HM, Woodfield SE, Chen Z, Bolduc C, Bergmann A. Common and distinct genetic properties of ESCRT-II components in Drosophila. PLoS One. 2009; 4(1):e4165. PMID: 19132102.
      Citations: 24     Fields:    Translation:AnimalsCells
    43. Xu D, Woodfield SE, Lee TV, Fan Y, Antonio C, Bergmann A. Genetic control of programmed cell death (apoptosis) in Drosophila. Fly (Austin). 2009 Jan-Mar; 3(1):78-90. PMID: 19182545.
      Citations: 65     Fields:    Translation:AnimalsCells
    44. Ditzel M, Broemer M, Tenev T, Bolduc C, Lee TV, Rigbolt KT, Elliott R, Zvelebil M, Blagoev B, Bergmann A, Meier P. Inactivation of effector caspases through nondegradative polyubiquitylation. Mol Cell. 2008 Nov 21; 32(4):540-53. PMID: 19026784.
      Citations: 59     Fields:    Translation:AnimalsCells
    45. Fan Y, Bergmann A. Apoptosis-induced compensatory proliferation. The Cell is dead. Long live the Cell! Trends Cell Biol. 2008 Oct; 18(10):467-73. PMID: 18774295.
      Citations: 135     Fields:    Translation:AnimalsCells
    46. Fan Y, Bergmann A. Distinct mechanisms of apoptosis-induced compensatory proliferation in proliferating and differentiating tissues in the Drosophila eye. Dev Cell. 2008 Mar; 14(3):399-410. PMID: 18331718.
      Citations: 118     Fields:    Translation:AnimalsCells
    47. Wang Y, Werz C, Xu D, Chen Z, Li Y, Hafen E, Bergmann A. Drosophila cbl is essential for control of cell death and cell differentiation during eye development. PLoS One. 2008 Jan 16; 3(1):e1447. PMID: 18197257.
      Citations: 13     Fields:    Translation:Animals
    48. Bergmann A. Autophagy and cell death: no longer at odds. Cell. 2007 Dec 14; 131(6):1032-4. PMID: 18083090.
      Citations: 37     Fields:    Translation:Animals
    49. Lee TV, Ding T, Chen Z, Rajendran V, Scherr H, Lackey M, Bolduc C, Bergmann A. The E1 ubiquitin-activating enzyme Uba1 in Drosophila controls apoptosis autonomously and tissue growth non-autonomously. Development. 2008 Jan; 135(1):43-52. PMID: 18045837.
      Citations: 38     Fields:    Translation:HumansAnimalsCells
    50. Mendes CS, Arama E, Brown S, Scherr H, Srivastava M, Bergmann A, Steller H, Mollereau B. Cytochrome c-d regulates developmental apoptosis in the Drosophila retina. EMBO Rep. 2006 Sep; 7(9):933-9. PMID: 16906130.
      Citations: 42     Fields:    Translation:Animals
    51. Bergmann A. IKK epsilon signaling: not just NF-kappaB. Curr Biol. 2006 Aug 08; 16(15):R588-90. PMID: 16890515.
      Citations: 1     Fields:    Translation:AnimalsCells
    52. Xu D, Wang Y, Willecke R, Chen Z, Ding T, Bergmann A. The effector caspases drICE and dcp-1 have partially overlapping functions in the apoptotic pathway in Drosophila. Cell Death Differ. 2006 Oct; 13(10):1697-706. PMID: 16645642.
      Citations: 53     Fields:    Translation:AnimalsCells
    53. Srivastava M, Scherr H, Lackey M, Xu D, Chen Z, Lu J, Bergmann A. ARK, the Apaf-1 related killer in Drosophila, requires diverse domains for its apoptotic activity. Cell Death Differ. 2007 Jan; 14(1):92-102. PMID: 16645639.
      Citations: 36     Fields:    Translation:AnimalsCells
    54. Herz HM, Chen Z, Scherr H, Lackey M, Bolduc C, Bergmann A. vps25 mosaics display non-autonomous cell survival and overgrowth, and autonomous apoptosis. Development. 2006 May; 133(10):1871-80. PMID: 16611691.
      Citations: 86     Fields:    Translation:AnimalsCells
    55. Arama E, Bader M, Srivastava M, Bergmann A, Steller H. The two Drosophila cytochrome C proteins can function in both respiration and caspase activation. EMBO J. 2006 Jan 11; 25(1):232-43. PMID: 16362035.
      Citations: 61     Fields:    Translation:AnimalsCells
    56. Werz C, Lee TV, Lee PL, Lackey M, Bolduc C, Stein DS, Bergmann A. Mis-specified cells die by an active gene-directed process, and inhibition of this death results in cell fate transformation in Drosophila. Development. 2005 Dec; 132(24):5343-52. PMID: 16280349.
      Citations: 16     Fields:    Translation:AnimalsCells
    57. Cashio P, Lee TV, Bergmann A. Genetic control of programmed cell death in Drosophila melanogaster. Semin Cell Dev Biol. 2005 Apr; 16(2):225-35. PMID: 15797833.
      Citations: 24     Fields:    Translation:AnimalsCells
    58. Xu D, Li Y, Arcaro M, Lackey M, Bergmann A. The CARD-carrying caspase Dronc is essential for most, but not all, developmental cell death in Drosophila. Development. 2005 May; 132(9):2125-34. PMID: 15800001.
      Citations: 97     Fields:    Translation:AnimalsCells
    59. Bergmann A, Yang AY, Srivastava M. Regulators of IAP function: coming to grips with the grim reaper. Curr Opin Cell Biol. 2003 Dec; 15(6):717-24. PMID: 14644196.
      Citations: 37     Fields:    Translation:AnimalsCells
    60. Sathyanarayana P, Barthwal MK, Lane ME, Acevedo SF, Skoulakis EM, Bergmann A, Rana A. Drosophila mixed lineage kinase/slipper, a missing biochemical link in Drosophila JNK signaling. Biochim Biophys Acta. 2003 Apr 07; 1640(1):77-84. PMID: 12676357.
      Citations: 14     Fields:    Translation:AnimalsCells
    61. Sathyanarayana P, Barthwal MK, Kundu CN, Lane ME, Bergmann A, Tzivion G, Rana A. Activation of the Drosophila MLK by ceramide reveals TNF-alpha and ceramide as agonists of mammalian MLK3. Mol Cell. 2002 Dec; 10(6):1527-33. PMID: 12504027.
      Citations: 48     Fields:    Translation:HumansAnimalsCells
    62. Ryoo HD, Bergmann A, Gonen H, Ciechanover A, Steller H. Regulation of Drosophila IAP1 degradation and apoptosis by reaper and ubcD1. Nat Cell Biol. 2002 Jun; 4(6):432-8. PMID: 12021769.
      Citations: 113     Fields:    Translation:AnimalsCells
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