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  • 1
    Publication Date: 2013-06-22
    Description: Adult stem cells are essential for tissue homeostasis and wound repair. Their proliferative capacity must be tightly regulated to prevent the emergence of unwanted and potentially dangerous cells, such as cancer cells. We found that mice deficient for the proapoptotic Sept4/ARTS gene have elevated numbers of hair follicle stem cells (HFSCs) that are protected against apoptosis. Sept4/ARTS(-/-) mice display marked improvement in wound healing and regeneration of hair follicles. These phenotypes depend on HFSCs, as indicated by lineage tracing. Inactivation of XIAP, a direct target of ARTS, abrogated these phenotypes and impaired wound healing. Our results indicate that apoptosis plays an important role in regulating stem cell-dependent regeneration and suggest that this pathway may be a target for regenerative medicine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4358763/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4358763/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fuchs, Yaron -- Brown, Samara -- Gorenc, Travis -- Rodriguez, Joe -- Fuchs, Elaine -- Steller, Hermann -- R01 AR050452/AR/NIAMS NIH HHS/ -- R01-AR050452/AR/NIAMS NIH HHS/ -- R01GM60124/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Jul 19;341(6143):286-9. doi: 10.1126/science.1233029. Epub 2013 Jun 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Strang Laboratory of Apoptosis and Cancer Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23788729" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/cytology/*physiology ; Animals ; Apoptosis/genetics/*physiology ; Hair Follicle/cytology/*physiology ; Inhibitor of Apoptosis Proteins/genetics ; Mice ; Mice, Mutant Strains ; Septins/genetics/*physiology ; Wound Healing/genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-01-24
    Description: Apoptosis, a form of cellular suicide, involves the activation of CED-3-related cysteine proteases (caspases). The regulation of caspases by apoptotic signals and the precise mechanism by which they kill the cell remain unknown. In Drosophila, different death-inducing stimuli induce the expression of the apoptotic activator reaper. Cell killing by reaper and two genetically linked apoptotic activators, hid and grim, requires caspase activity. A Drosophila caspase, named Drosophila caspase-1 (DCP-1), was identified and found to be structurally and biochemically similar to Caenorhabditis elegans CED-3. Loss of zygotic DCP-1 function in Drosophila caused larval lethality and melanotic tumors, showing that this gene is essential for normal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Z -- McCall, K -- Steller, H -- New York, N.Y. -- Science. 1997 Jan 24;275(5299):536-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999799" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; Caenorhabditis elegans Proteins ; *Caspases ; Cloning, Molecular ; Cysteine Endopeptidases/chemistry/genetics/*metabolism ; DNA Fragmentation ; DNA Transposable Elements ; Drosophila/embryology/*enzymology/genetics ; Drosophila Proteins ; Embryo, Nonmammalian/enzymology ; Gene Deletion ; Genes, Insect ; HeLa Cells ; Helminth Proteins/chemistry/metabolism ; Humans ; Molecular Sequence Data ; Mutation ; RNA, Messenger/genetics/metabolism ; Sequence Homology, Amino Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-01-31
    Description: Caspases, a class of cysteine proteases, are an essential component of the apoptotic cell death program. During Drosophila oogenesis, nurse cells transfer their cytoplasmic contents to developing oocytes and then die. Loss of function for the dcp-1 gene, which encodes a caspase, caused female sterility by inhibiting this transfer. dcp-1- nurse cells were defective in the cytoskeletal reorganization and nuclear breakdown that normally accompany this process. The dcp-1- phenotype suggests that the cytoskeletal and nuclear events in the nurse cells make use of the machinery normally associated with apoptosis and that apoptosis of the nurse cells is a necessary event for oocyte development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCall, K -- Steller, H -- New York, N.Y. -- Science. 1998 Jan 9;279(5348):230-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biology, 31 Ames Street, 68-430, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9422696" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/analysis ; Animals ; Apoptosis ; *Caspases ; Cell Membrane/chemistry ; Cysteine Endopeptidases/genetics/*metabolism ; Cytoplasm/chemistry ; Cytoskeleton/chemistry/physiology ; Drosophila/enzymology/*physiology ; Drosophila Proteins ; Female ; Lamins ; Mutation ; Nuclear Envelope/metabolism ; Nuclear Proteins/analysis/metabolism ; Oocytes/*physiology ; *Oogenesis ; Ovary/cytology/enzymology ; Phenotype
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1996-02-09
    Description: The reaper gene (rpr) is important for the activation of apoptosis in Drosophila. To investigate whether rpr expression is sufficient to induce apoptosis, transgenic flies were generated that express rpr complementary DNA or the rpr open reading frame in cells that normally live. Transcription of rpr from a heat-inducible promoter rapidly caused wide-spread ectopic apoptosis and organismal death. Ectopic overexpression of rpr in the developing retina resulted in eye ablation. The occurrence of cell death was highly sensitive to the dosage of the transgene. Because cell death induced by the protein encoded by rpr (RPR) could be blocked by the baculovirus p35 protein, RPR appears to activate a death program mediated by a ced-3/ICE (interleukin-1 converting enzyme)-like protease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, K -- Tahaoglu, E -- Steller, H -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):805-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cutaneous Biology Research Center, Massachusetts General Hospital, Charlestown 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8628996" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; *Apoptosis ; Caspase 1 ; Cysteine Endopeptidases/metabolism ; DNA, Complementary/genetics ; Drosophila/cytology/embryology/*genetics ; *Drosophila Proteins ; Gene Dosage ; Gene Expression ; *Genes, Insect ; Hot Temperature ; Inhibitor of Apoptosis Proteins ; Mutation ; Open Reading Frames ; Peptides/*genetics/physiology ; Photoreceptor Cells, Invertebrate/cytology ; Transgenes ; Viral Proteins/genetics/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1995-03-10
    Description: Apoptosis is a morphologically distinct form of programmed cell death that plays a major role during development, homeostasis, and in many diseases including cancer, acquired immunodeficiency syndrome, and neurodegenerative disorders. Apoptosis occurs through the activation of a cell-intrinsic suicide program. The basic machinery to carry out apoptosis appears to be present in essentially all mammalian cells at all times, but the activation of the suicide program is regulated by many different signals that originate from both the intracellular and the extracellular milieu. Genetic studies in the nematode Caenorhabditis elegans and in the fruit fly Drosophila melanogaster have led to the isolation of genes that are specifically required for the induction of programmed cell death. At least some components of the apoptotic program have been conserved among worms, insects, and vertebrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steller, H -- New York, N.Y. -- Science. 1995 Mar 10;267(5203):1445-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7878463" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis/genetics/physiology ; Caenorhabditis elegans/cytology/genetics ; Cysteine Endopeptidases/genetics/metabolism ; Drosophila/cytology/genetics ; *Drosophila Proteins ; Gene Expression Regulation ; *Genes, Helminth ; *Genes, Insect ; Peptides/genetics/physiology ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1994-04-29
    Description: A gene, reaper (rpr), that appears to play a central control function for the initiation of programmed cell death (apoptosis) in Drosophila was identified. Virtually all programmed cell death that normally occurs during Drosophila embryogenesis was blocked in embryos homozygous for a small deletion that includes the reaper gene. Mutant embryos contained many extra cells and failed to hatch, but many other aspects of development appeared quite normal. Deletions that include reaper also protected embryos from apoptosis caused by x-irradiation and developmental defects. However, high doses of x-rays induced some apoptosis in mutant embryos, and the resulting corpses were phagocytosed by macrophages. These data suggest that the basic cell death program is intact although it was not activated in mutant embryos. The DNA encompassed by the deletion was cloned and the reaper gene was identified on the basis of the ability of cloned DNA to restore apoptosis to cell death defective embryos in germ line transformation experiments. The reaper gene appears to encode a small peptide that shows no homology to known proteins, and reaper messenger RNA is expressed in cells destined to undergo apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, K -- Grether, M E -- Abrams, J M -- Young, L -- Farrell, K -- Steller, H -- 5 F32 NS08536/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):677-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Brain and Cognitive Sciences, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171319" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis/*genetics ; Base Sequence ; Cloning, Molecular ; DNA Primers ; Drosophila/cytology/embryology/*genetics ; *Drosophila Proteins ; Embryo, Nonmammalian/cytology ; *Genes, Insect ; Models, Genetic ; Molecular Sequence Data ; Mutation ; Nervous System/cytology ; Neurons/cytology ; Peptides/chemistry/*genetics/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Developmental Biology 109 (1985), S. 54-62 
    ISSN: 0012-1606
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 8
    Publication Date: 2008-09-08
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 9
    Publication Date: 1993-08-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 10
    Publication Date: 1992-11-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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