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Artykuły w czasopismach na temat "Apoptosis"
Cutrona, Giovanna, Nicolò Leanza, Massimo Ulivi, Giovanni Melioli, Vito L. Burgio, Giovanni Mazzarello, Giovanni Gabutti, Silvio Roncella i Manlio Ferrarini. "Expression of CD10 by Human T Cells That Undergo Apoptosis Both In Vitro and In Vivo". Blood 94, nr 9 (1.11.1999): 3067–76. http://dx.doi.org/10.1182/blood.v94.9.3067.
Pełny tekst źródłaCutrona, Giovanna, Nicolò Leanza, Massimo Ulivi, Giovanni Melioli, Vito L. Burgio, Giovanni Mazzarello, Giovanni Gabutti, Silvio Roncella i Manlio Ferrarini. "Expression of CD10 by Human T Cells That Undergo Apoptosis Both In Vitro and In Vivo". Blood 94, nr 9 (1.11.1999): 3067–76. http://dx.doi.org/10.1182/blood.v94.9.3067.421a32_3067_3076.
Pełny tekst źródłaPark, Cheol, Cheng-Yun Jin, Tae Hyun Choi, Su Hyun Hong i Yung Hyun Choi. "Effect of Proapoptotic Bcl-2 on Naringenin-induced Apoptosis in Human Leukemia U937 Cells". Journal of Life Science 23, nr 9 (30.09.2013): 1118–25. http://dx.doi.org/10.5352/jls.2013.23.9.1118.
Pełny tekst źródłaLizama, Carlos, Diego Rojas-Benítez, Marcelo Antonelli, Andreas Ludwig, Ximena Bustamante-Marín, Jurriaan Brouwer-Visser i Ricardo D. Moreno. "TACE/ADAM17 is involved in germ cell apoptosis during rat spermatogenesis". REPRODUCTION 140, nr 2 (sierpień 2010): 305–17. http://dx.doi.org/10.1530/rep-10-0104.
Pełny tekst źródłaGETTI, G. T., R. A. CHEKE i D. P. HUMBER. "Induction of apoptosis in host cells: a survival mechanism forLeishmaniaparasites?" Parasitology 135, nr 12 (8.09.2008): 1391–99. http://dx.doi.org/10.1017/s0031182008004915.
Pełny tekst źródłaLangrová, Tereza, Zbyšek Sládek i Dušan Ryšánek. "The effect of the bacterial pathogens Staphylococcus aureus and Streptococcus uberis on morphological features of apoptosis of heifers mammary gland neutrophils". Acta Universitatis Agriculturae et Silviculturae Mendelianae Brunensis 53, nr 4 (2005): 61–74. http://dx.doi.org/10.11118/actaun200553040061.
Pełny tekst źródłaAravani, Dimitra, Kirsty Foote, Nichola Figg, Alison Finigan, Anna Uryga, Murray Clarke i Martin Bennett. "Cytokine regulation of apoptosis-induced apoptosis and apoptosis-induced cell proliferation in vascular smooth muscle cells". Apoptosis 25, nr 9-10 (5.07.2020): 648–62. http://dx.doi.org/10.1007/s10495-020-01622-4.
Pełny tekst źródłaHassan, Mohamed, Hidemichi Watari, Ali AbuAlmaaty, Yusuke Ohba i Noriaki Sakuragi. "Apoptosis and Molecular Targeting Therapy in Cancer". BioMed Research International 2014 (12.06.2014): 1–23. http://dx.doi.org/10.1155/2014/150845.
Pełny tekst źródłaLaBelle, James L., Jill K. Fisher, Samuel G. Katz, Gregory H. Bird, Chelsea E. Lawrence, Amy M. Silverstein i Loren D. Walensky. "Pharmacologic Replacement of BIM BH3 Reactivates Apoptosis in Hematologic Cancer and Lymphoproliferative Disease." Blood 110, nr 11 (16.11.2007): 524. http://dx.doi.org/10.1182/blood.v110.11.524.524.
Pełny tekst źródłaResanović, Ivana, Emina Sudar-Milovanović, Nikola Bogdanović, Aleksandra Jovanović, Sonja Zafirović, Anastasija Panić i Esma Isenović. "Fundamentals of apoptosis". Medicinska istrazivanja 49, nr 3 (2015): 42–45. http://dx.doi.org/10.5937/medist1502042r.
Pełny tekst źródłaRozprawy doktorskie na temat "Apoptosis"
Heiligtag, Sven. "Induction of apoptosis in neuroblastoma analysis of apoptotic pathways and putative apoptosis-mediating receptors /". [S.l.] : [s.n.], 2001. http://www.sub.uni-hamburg.de/disse/464/Disse.pdf.
Pełny tekst źródłaDevore, Casey Leigh. "DNR1 Regulates apoptosis: new insights into mosquito apoptosis". Thesis, Kansas State University, 2009. http://hdl.handle.net/2097/11972.
Pełny tekst źródłaDepartment of Biology
Rollie Clem
Apoptosis, or programmed cell death, is a crucial conserved process among organisms for deleting damaged unwanted cells, as well as for development and viral defense, and plays an important role in multiple diseases. Too much apoptosis may lead to Alzheimer’s disease, and too little may result in cancer. Therefore, the ability to understand this process is essential for improved medical knowledge today. Apoptosis has been explored in a number of species and pathways seem relatively conserved among most, with unique aspects contained in each, but little is known about apoptosis in mosquitoes. Improved knowledge and growing interest concerning apoptosis in mosquitoes is necessary considering the vast health effects seen across the globe as a result of diseases transferred by the mosquito vector. The Dengue virus mosquito vector Aedes aegypti was the focus here. A new player named defense repressor 1 was discovered in Drosophila melanogaster (DmDnr1), shown to play a role in apoptosis, and the homolog discovered in A. aegypti (AeDnr1). Silencing Dmdnr1 resulted in cells sensitized to apoptosis but was not enough to induce spontaneous apoptosis. In contrast, silencing Aednr1 in the A. aegypti cell line, Aag2, led to spontaneously induced apoptosis. This showed the importance of AeDnr1 as a member of the apoptotic pathway in this species. Epistasis experiments showed that apoptosis induced by silencing Aednr1 requires the initiator caspase Dronc and the effector caspase CASPS8, whereas apoptosis induced by silencing the inhibitor of apoptosis, Aeiap1, also requires Dronc but acts through the effector caspase CASPS7. Further epistasis experiments showed that apoptosis induced by silencing Aednr1 requires the IAP antagonist Mx, but not IMP. This showed for the first time a gene regulating upstream of an IAP antagonist. Biochemical studies showed that AeDnr1 regulates active CASPS8 but not CASPS7, and interacts with Mx and CASPS8 but not AeDronc, CASPS7 nor AeIAP1. Studies also showed Mx competes effectively with CASPS8 but not CASPS7 for AeIAP1 binding, and IMP competes effectively with CASPS7 but not CASPS8 for AeIAP1 binding. An improved apoptosis pathway for the mosquito A. aegypti emerged involving a potential feedback loop with explanations for the upstream IAP antagonist preference as well as the downstream effector caspase preference resulting from apoptosis induced by Aednr1 silencing. Through the discussed research, multiple unique findings resulted. Studying the mosquito model will allow us to find certain gene relations that are more difficult to uncover in the Drosophila model. Because Dnr1 is found in most systems, this improved pathway may shed light not only on a potential role of Dnr1 in apoptosis in insects but higher organisms as well.
Seton, Kristina. "Eosinophil Apoptosis". Doctoral thesis, Uppsala University, Department of Medical Sciences, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3427.
Pełny tekst źródłaApoptosis or programmed cell death is crucial for the resolution of inflammation, and phagocytosis of apoptotic cells initiates the release of actively anti-inflammatory responses from the phagocytes. Eosinophils are one of the most potent inflammatory cells in the body and is involved in a number of diseases, most commonly associated with parasitic infections and allergic diseases. Apoptosis in eosinophils is therefore one of the most important systems to avoid inflammation. This aim of the present investigation was to examine the mechanisms behind, and the consequences of this process in eosinophils. Apoptotic eosinophils have a unique surface receptor expression that indicates abilities to communicate with T-, B- and antigen presenting cells. They have a novel expression of CD49f, indicating an importance for binding to laminin or unknown functions of the VLA-6 receptor, possibly in the concept of phagocytosis of the apoptotic cell.
In apoptotic eosinophils the granules are translocated to the periphery of the cell, probably through a disruption of the cytoskeleton. This translocation makes the granules easily accessible and the apoptotic eosinophil can release considerable amounts of granule proteins in response to specific stimuli. The spontaneous release however, is decreased as compared with living cells.
Furthermore, the survival of eosinophils in response to an allergen challenge is increased in healthy subjects, but not in allergic patients. Mechanistically, this needs further investigation, but one theory is that it is due to the presence of specific IgE in patients in combination with differences in the response from the epithelial cells.
Quarrie, Lynda H. "Mammary apoptosis". Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318886.
Pełny tekst źródłaJoza, Nicholas. "Differential requirement for the mitochondrial apoptosis-inducing factor in apoptotic pathways". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63071.pdf.
Pełny tekst źródłaSani, Marc-Antoine. "Apoptosis Regulation via the Mitochondrial Pathway : Membrane Response upon Apoptotic Stimuli". Doctoral thesis, Umeå universitet, Kemiska institutionen, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1883.
Pełny tekst źródłaSani, Marc Antoine. "Apoptosis regulation via the mitochondrial pathway : membrane response upon apoptotic stimuli". Thesis, Bordeaux 1, 2008. http://www.theses.fr/2008BOR13651/document.
Pełny tekst źródłaThe aim of this thesis was the investigation of the mitochondrial response mechanisms upon apoptotic stimuli. The specific objectives were the biophysical characterization of membrane dynamics and the specific roles of lipids in the context of apoptotic regulation occurring at the mitochondrion and its complex membrane systems. The BH4 domain is an anti-apoptotic specific domain of the Bcl-2 protein. Solid phase peptide synthesis was used to produce large amount of the peptide for biophysical studies. A protocol has been established and optimized, guarantying the required purity for biophysical studies. In detail the purification by high performance liquid chromatography and the characterisation via mass spectroscopy are described. The secondary structure of BH4 changes significantly in the presence of lipid vesicles as observed by infrared spectroscopy and circular dichroism. The BH4 peptide aggregates at the membrane surface and inserts slightly into the hydrophobic part of the membrane. Using nuclear magnetic resonance (NMR) and calorimetry techniques, it could even be shown that the BH4 domain modifies the dynamic and organization of the liposomes which mimic a mitochondrial surface. The second study was on the first helix of the pro-apoptotic protein Bax. This sequence called Bax-a1 has the function to address the cytosolic Bax protein to the mitochondrial membrane upon activation. Once again a protocol has been established for the synthesis and purification of this peptide. The aim was to elucidate the key role of cardiolipin, a mitochondria-specific phospholipid, in the interaction of Bax-a1 with the mitochondrial membrane system. The NMR and circular dichroism studies showed that Bax-a1 interacts with the membrane models only if they contain the cardiolipin, producing a strong electrostatic lock effect which is located at the membrane surface. Finally, a new NMR approach was developed which allows the investigation of the lipid response of isolated active mitochondria upon the presence of apoptotic stimuli. The goal was there to directly monitor lipid specific the occurring changes during these physiological activities
Schmeiser, Katja. "Expression of apoptosis specific proteins (ASPs) during apoptosis and autophagy". Thesis, University of Birmingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394165.
Pełny tekst źródłaCabezas, Somalo Maria. "Polimorfismes genètics i tractament antitumoral: evolució dels pacients amb leucèmia limfoblàstica aguda i inducció de leucèmies secundàries". Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/458541.
Pełny tekst źródłaChildren with acute lymphoblastic leukemia (ALL) respond differently to chemotherapy. Genetic polymorphisms together with genetic abnormalities in leukemic cells are probably behind variability in response to chemotherapy in childhood ALL. In the present thesis, we investigated whether copy number variants and/or single nucleotide polymorphism (SNPs) in genes coding for proteins involved in drug metabolism or apoptosis (CYP2D6, GSTT1, GSTM1, SULT1A1, UGT2B17 and TP53) have an impact on the therapeutic outcome of childhood ALL. We observed that patients with GSTM1 non-null genotype showed poor survival and patients carrying at least one allele of the Pro variant of the TP53 Arg72Pro SNP also showed a tendency to poor survival. When combining GSTM1 and TP53 genotypes, our data indicated that they can predict survival with higher significance than GSTM1 alone. To validate these results, an in vitro model was created with leukemic Jurkat cell line by transfection of the two TP53 variants at codon 72, either Pro or Arg and a GSTM1 siRNA into Jurkat cells. Results revealed that Jurkat p53Arg GSTM1 null cells exhibited higher sensitivity to dexamethasone, confirming the results observed in patients. It has been reported that GSTM1 inhibits glucocorticoids-induced cell death and that p53Arg induces apoptosis more efficiently than p53Pro, which is a more efficient activator of cell cycle arrest and DNA damage repair. Therefore, at least one copy of the gene GSTM1 and p53Pro, enough in heterozygosis, would lead to less efficient apoptosis in leukemic cells after the antileukemic treatment and could therefore be related to lower survival. On the other hand, one of the most severe complications after successful cancer therapy is the development of a secondary cancer, mostly a myeloid neoplasm (t-MN). Up to 20% of patients treated for a primary cancer develop t-MN. Constitutional genetic variation is likely to impact on an individual’s risk of developing t-MN. In the present thesis, we analyzed the impact of two polymorphisms in the p53 pathway on the development of t-MN. Results revealed that the TP53 Arg72Pro polymorphism and the MDM2 SNP309 were associated with t-MN risk. The p53Pro and the G allele of MDM2 were overrepresented in t-MN patients. To assess the biological effect of the TP53 polymorphism, we established Jurkat isogenic cell lines expressing p53Arg or p53Pro and assessed the number of γ-H2AX foci, chromosome alterations, sister chromatid exchanges, and apoptotic cells, as well as development of chromosomal alterations typical of t-MN, after treatment with an alkylating agent, or a topoisomerase II poison. Jurkat p53Arg cells presented more γ-H2AX foci per cell, higher level of DNA damage and higher apoptotic potential than p53Pro cells. Moreover, Jurkat p53Pro cells presented the t(15;17) translocation and 5q33 deletion whereas Jurkat p53Arg cells did not present the alterations. Therefore, it could be possible that differences in t-MN risk in patients treated with the same doses of chemotherapy and/or radiation are due to the ability of individuals to undergo apoptosis or to repair DNA lesions more or less efficiently related to the TP53 polymorphism.
Deng, Diana Xi. "Metallothionein and apoptosis". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq21105.pdf.
Pełny tekst źródłaKsiążki na temat "Apoptosis"
Erhardt, Peter, i Ambrus Toth, red. Apoptosis. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-017-5.
Pełny tekst źródłaAl-Rubeai, M., red. Apoptosis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102303.
Pełny tekst źródłaReed, John C., i Douglas R. Green, red. Apoptosis. Cambridge: Cambridge University Press, 2011. http://dx.doi.org/10.1017/cbo9780511976094.
Pełny tekst źródłaKuchino, Y., i W. E. G. Müller, red. Apoptosis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4.
Pełny tekst źródłaMihich, Enrico, i Robert T. Schimke, red. Apoptosis. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-9217-1.
Pełny tekst źródłaD, Jacobson Michael, i McCarthy Nicola J, red. Apoptosis. Oxford, OX: Oxford University Press, 2002.
Znajdź pełny tekst źródłaPérez, Lidia Gómez. Apoptosis. [Madrid]: Legados Ediciones, 2015.
Znajdź pełny tekst źródłaR, Preedy Victor, red. Apoptosis. Enfield NH: Science Publishers, 2010.
Znajdź pełny tekst źródłaR, Preedy Victor, red. Apoptosis. Enfield, N.H: Science Publishers, 2010.
Znajdź pełny tekst źródła1948-, Al-Rubeai Mohamed, red. Apoptosis. Berlin: Springer, 1998.
Znajdź pełny tekst źródłaCzęści książek na temat "Apoptosis"
McKenna, Sharon L., Adrian J. McGowan i Thomas G. Cotter. "Molecular mechanisms of programmed cell death". W Apoptosis, 1–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102304.
Pełny tekst źródłaDarzynkiewicz, Zbigniew, i Frank Traganos. "Measurement of apoptosis". W Apoptosis, 33–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102305.
Pełny tekst źródłaBruckheimer, E. M., S. H. Cho, M. Sarkiss, J. Herrmann i T. J. McDonnell. "The Bcl-2 gene family and apoptosis". W Apoptosis, 75–105. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102306.
Pełny tekst źródłaHarvey, Natasha L., i Sharad Kumar. "The role of caspases in apoptosis". W Apoptosis, 107–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102307.
Pełny tekst źródłaAutuori, Francesco, Maria Grazia Farrace, Serafina Oliverio, Lucia Piredda i Mauro Piacentini. "“Tissue” transglutaminase and apoptosis". W Apoptosis, 129–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102308.
Pełny tekst źródłaO'Connor, Rosemary. "Survival factors and apoptosis". W Apoptosis, 137–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102309.
Pełny tekst źródłaSingh, R. P., i M. Al-Rubeai. "Apoptosis and bioprocess technology". W Apoptosis, 167–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102310.
Pełny tekst źródłaTanuma, S., i D. Shiokawa. "An Endonuclease Responsible for Apoptosis". W Apoptosis, 1–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4_1.
Pełny tekst źródłaRojko, J. L., J. R. Hartke, C. M. Cheney, A. J. Phipps i J. C. Neil. "Cytopathic Feline Leukemia Viruses Cause Apoptosis in Hemolymphatic Cells". W Apoptosis, 13–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4_2.
Pełny tekst źródłaMüller, W. E. G., G. Pergande, H. Ushijima, C. Schleger, M. Kelve i S. Perovic. "Neurotoxicity in Rat Cortical Cells Caused by N-Methyl-D-Aspartate (NMDA) and gp120 of HIV-1: Induction and Pharmacological Intervention". W Apoptosis, 44–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4_3.
Pełny tekst źródłaStreszczenia konferencji na temat "Apoptosis"
van der Meer, Freek J., Dirk J. Faber, Riëtte de Bruin, Maurice C. Aalders, Jop Perrée i Ton G. van Leeuwen. "Changes in optical properties of cells and tissue after induction of apoptosis". W European Conference on Biomedical Optics. Washington, D.C.: Optica Publishing Group, 2001. http://dx.doi.org/10.1364/ecbo.2001.4431_122.
Pełny tekst źródłaZhao, Ruogang, Lina Lin i Craig A. Simmons. "The Effects of Cell Contraction and Loss of Adhesion on the Apoptosis of Valve Interstitial Cells". W ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19249.
Pełny tekst źródłaKuttikrishnan, Shilpa, Kirti S. Prabhu, Tamam Elimat, Ashraf Khalil, Nicholas H. Oberlies, Feras Q. Alali i Shahab Uddin. "Anticancer Activity of Neosetophomone B, An Aquatic Fungal Secondary Metabolite, Against Hematological Malignancie S". W Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0106.
Pełny tekst źródłaDereli-Korkut, Zeynep, i Sihong Wang. "Microfluidic Cell Arrays to Mimic 3D Tissue Microenvironment". W ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80411.
Pełny tekst źródłaBaust, John M., Robert G. Van Buskirk i John G. Baust. "Cryopreservation of an Engineered Skin Equivalent: The Apoptosis Paradigm". W ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0586.
Pełny tekst źródłaТрушина, Элеонора Николаевна. "APOPTOSIS OF BRAIN NEURONS IN ISCHEMIA". W Психология. Спорт. Здравоохранение: сборник избранных статей по материалам Международной научной конференции (Санкт-Петербург, Апрель 2021). Crossref, 2021. http://dx.doi.org/10.37539/psm296.2021.47.78.003.
Pełny tekst źródłaLiu, Lei, Yingjie Zhang i Xianwang Wang. "Involvement of caspase-dependent and -independent apoptotic pathways in cisplatin-induced apoptosis". W SPIE BiOS: Biomedical Optics, redaktor Wei R. Chen. SPIE, 2009. http://dx.doi.org/10.1117/12.808431.
Pełny tekst źródłaCheng, Chao-Min, i Philip R. LeDuc. "Effects of Local Mechanical Stimulation on Cellular Behavior". W ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176082.
Pełny tekst źródła"APOPTOSIS AND ASSESSMENT OF CYTOGENETIC DISORDERS APOPTOSIS AND ASSESSMENT OF CYTOGENETIC DISORDERS IN THE POPULATION OF THE ARCTIC ZONE OF THE RUSSIAN FEDERATION". W СОВРЕМЕННЫЕ ПРОБЛЕМЫ ЭКОЛОГИИ И ЗДОРОВЬЯ НАСЕЛЕНИЯ. ЭКОЛОГИЯ И ЗДОРОВЬЕ НАСЕЛЕНИЯ. Иркутский научный центр хирургии и травматологии, 2023. http://dx.doi.org/10.12731/978-5-98277-383-8-art1.
Pełny tekst źródłaKessel, David, Yu Luo i Hyeong-Reh C. Kim. "Determinants of PDT-induced apoptosis". W BiOS 2000 The International Symposium on Biomedical Optics, redaktor Thomas J. Dougherty. SPIE, 2000. http://dx.doi.org/10.1117/12.379884.
Pełny tekst źródłaRaporty organizacyjne na temat "Apoptosis"
Donato, Nicholas J. Calcium-Mediated Apoptosis and Apoptotic Sensitization in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2003. http://dx.doi.org/10.21236/ada418675.
Pełny tekst źródłaHolley, Christopher L. Reaper-Induced Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2002. http://dx.doi.org/10.21236/ada411241.
Pełny tekst źródłaPerry, Jennifer. Reaper-Induced Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2005. http://dx.doi.org/10.21236/ada462723.
Pełny tekst źródłaKornbluth, Sally A., i Erica K. Evans. Regulation of Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 1999. http://dx.doi.org/10.21236/ada381256.
Pełny tekst źródłaLiu, Junwei. Apoptosis-Dependent and Apoptosis-Independent Functions Bim in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, marzec 2004. http://dx.doi.org/10.21236/ada439201.
Pełny tekst źródłaMarcelli, Marco. Apoptosis in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2001. http://dx.doi.org/10.21236/ada398042.
Pełny tekst źródłaMarcelli, Marco. Apoptosis in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2002. http://dx.doi.org/10.21236/ada407231.
Pełny tekst źródłaVogel, Kristine S. Neurofibromin and Neuronal Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2004. http://dx.doi.org/10.21236/ada429612.
Pełny tekst źródłaVogel, Kristine S. Neurofibromin and Neuronal Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2003. http://dx.doi.org/10.21236/ada420881.
Pełny tekst źródłaZhang, Hong. A Novel Apoptosis Regulator. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2000. http://dx.doi.org/10.21236/ada390571.
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