Academic literature on the topic 'Apoptosis'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Apoptosis.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Apoptosis"
Cutrona, Giovanna, Nicolò Leanza, Massimo Ulivi, Giovanni Melioli, Vito L. Burgio, Giovanni Mazzarello, Giovanni Gabutti, Silvio Roncella, and Manlio Ferrarini. "Expression of CD10 by Human T Cells That Undergo Apoptosis Both In Vitro and In Vivo." Blood 94, no. 9 (November 1, 1999): 3067–76. http://dx.doi.org/10.1182/blood.v94.9.3067.
Full textCutrona, Giovanna, Nicolò Leanza, Massimo Ulivi, Giovanni Melioli, Vito L. Burgio, Giovanni Mazzarello, Giovanni Gabutti, Silvio Roncella, and Manlio Ferrarini. "Expression of CD10 by Human T Cells That Undergo Apoptosis Both In Vitro and In Vivo." Blood 94, no. 9 (November 1, 1999): 3067–76. http://dx.doi.org/10.1182/blood.v94.9.3067.421a32_3067_3076.
Full textPark, Cheol, Cheng-Yun Jin, Tae Hyun Choi, Su Hyun Hong, and Yung Hyun Choi. "Effect of Proapoptotic Bcl-2 on Naringenin-induced Apoptosis in Human Leukemia U937 Cells." Journal of Life Science 23, no. 9 (September 30, 2013): 1118–25. http://dx.doi.org/10.5352/jls.2013.23.9.1118.
Full textLizama, Carlos, Diego Rojas-Benítez, Marcelo Antonelli, Andreas Ludwig, Ximena Bustamante-Marín, Jurriaan Brouwer-Visser, and Ricardo D. Moreno. "TACE/ADAM17 is involved in germ cell apoptosis during rat spermatogenesis." REPRODUCTION 140, no. 2 (August 2010): 305–17. http://dx.doi.org/10.1530/rep-10-0104.
Full textGETTI, G. T., R. A. CHEKE, and D. P. HUMBER. "Induction of apoptosis in host cells: a survival mechanism forLeishmaniaparasites?" Parasitology 135, no. 12 (September 8, 2008): 1391–99. http://dx.doi.org/10.1017/s0031182008004915.
Full textLangrová, Tereza, Zbyšek Sládek, and 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, no. 4 (2005): 61–74. http://dx.doi.org/10.11118/actaun200553040061.
Full textAravani, Dimitra, Kirsty Foote, Nichola Figg, Alison Finigan, Anna Uryga, Murray Clarke, and Martin Bennett. "Cytokine regulation of apoptosis-induced apoptosis and apoptosis-induced cell proliferation in vascular smooth muscle cells." Apoptosis 25, no. 9-10 (July 5, 2020): 648–62. http://dx.doi.org/10.1007/s10495-020-01622-4.
Full textHassan, Mohamed, Hidemichi Watari, Ali AbuAlmaaty, Yusuke Ohba, and Noriaki Sakuragi. "Apoptosis and Molecular Targeting Therapy in Cancer." BioMed Research International 2014 (June 12, 2014): 1–23. http://dx.doi.org/10.1155/2014/150845.
Full textLaBelle, James L., Jill K. Fisher, Samuel G. Katz, Gregory H. Bird, Chelsea E. Lawrence, Amy M. Silverstein, and Loren D. Walensky. "Pharmacologic Replacement of BIM BH3 Reactivates Apoptosis in Hematologic Cancer and Lymphoproliferative Disease." Blood 110, no. 11 (November 16, 2007): 524. http://dx.doi.org/10.1182/blood.v110.11.524.524.
Full textResanović, Ivana, Emina Sudar-Milovanović, Nikola Bogdanović, Aleksandra Jovanović, Sonja Zafirović, Anastasija Panić, and Esma Isenović. "Fundamentals of apoptosis." Medicinska istrazivanja 49, no. 3 (2015): 42–45. http://dx.doi.org/10.5937/medist1502042r.
Full textDissertations / Theses on the topic "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.
Full textDevore, Casey Leigh. "DNR1 Regulates apoptosis: new insights into mosquito apoptosis." Thesis, Kansas State University, 2009. http://hdl.handle.net/2097/11972.
Full textDepartment 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.
Full textApoptosis 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.
Full textJoza, 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.
Full textSani, 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.
Full textSani, Marc Antoine. "Apoptosis regulation via the mitochondrial pathway : membrane response upon apoptotic stimuli." Thesis, Bordeaux 1, 2008. http://www.theses.fr/2008BOR13651/document.
Full textThe 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.
Full textCabezas, 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.
Full textChildren 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.
Full textBooks on the topic "Apoptosis"
Erhardt, Peter, and Ambrus Toth, eds. Apoptosis. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-017-5.
Full textAl-Rubeai, M., ed. Apoptosis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102303.
Full textReed, John C., and Douglas R. Green, eds. Apoptosis. Cambridge: Cambridge University Press, 2011. http://dx.doi.org/10.1017/cbo9780511976094.
Full textKuchino, Y., and W. E. G. Müller, eds. Apoptosis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4.
Full textMihich, Enrico, and Robert T. Schimke, eds. Apoptosis. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-9217-1.
Full textD, Jacobson Michael, and McCarthy Nicola J, eds. Apoptosis. Oxford, OX: Oxford University Press, 2002.
Find full textPérez, Lidia Gómez. Apoptosis. [Madrid]: Legados Ediciones, 2015.
Find full textR, Preedy Victor, ed. Apoptosis. Enfield NH: Science Publishers, 2010.
Find full textR, Preedy Victor, ed. Apoptosis. Enfield, N.H: Science Publishers, 2010.
Find full text1948-, Al-Rubeai Mohamed, ed. Apoptosis. Berlin: Springer, 1998.
Find full textBook chapters on the topic "Apoptosis"
McKenna, Sharon L., Adrian J. McGowan, and Thomas G. Cotter. "Molecular mechanisms of programmed cell death." In Apoptosis, 1–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102304.
Full textDarzynkiewicz, Zbigniew, and Frank Traganos. "Measurement of apoptosis." In Apoptosis, 33–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102305.
Full textBruckheimer, E. M., S. H. Cho, M. Sarkiss, J. Herrmann, and T. J. McDonnell. "The Bcl-2 gene family and apoptosis." In Apoptosis, 75–105. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102306.
Full textHarvey, Natasha L., and Sharad Kumar. "The role of caspases in apoptosis." In Apoptosis, 107–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102307.
Full textAutuori, Francesco, Maria Grazia Farrace, Serafina Oliverio, Lucia Piredda, and Mauro Piacentini. "“Tissue” transglutaminase and apoptosis." In Apoptosis, 129–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102308.
Full textO'Connor, Rosemary. "Survival factors and apoptosis." In Apoptosis, 137–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102309.
Full textSingh, R. P., and M. Al-Rubeai. "Apoptosis and bioprocess technology." In Apoptosis, 167–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102310.
Full textTanuma, S., and D. Shiokawa. "An Endonuclease Responsible for Apoptosis." In Apoptosis, 1–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4_1.
Full textRojko, J. L., J. R. Hartke, C. M. Cheney, A. J. Phipps, and J. C. Neil. "Cytopathic Feline Leukemia Viruses Cause Apoptosis in Hemolymphatic Cells." In Apoptosis, 13–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4_2.
Full textMüller, W. E. G., G. Pergande, H. Ushijima, C. Schleger, M. Kelve, and S. Perovic. "Neurotoxicity in Rat Cortical Cells Caused by N-Methyl-D-Aspartate (NMDA) and gp120 of HIV-1: Induction and Pharmacological Intervention." In Apoptosis, 44–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4_3.
Full textConference papers on the topic "Apoptosis"
van der Meer, Freek J., Dirk J. Faber, Riëtte de Bruin, Maurice C. Aalders, Jop Perrée, and Ton G. van Leeuwen. "Changes in optical properties of cells and tissue after induction of apoptosis." In European Conference on Biomedical Optics. Washington, D.C.: Optica Publishing Group, 2001. http://dx.doi.org/10.1364/ecbo.2001.4431_122.
Full textZhao, Ruogang, Lina Lin, and Craig A. Simmons. "The Effects of Cell Contraction and Loss of Adhesion on the Apoptosis of Valve Interstitial Cells." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19249.
Full textKuttikrishnan, Shilpa, Kirti S. Prabhu, Tamam Elimat, Ashraf Khalil, Nicholas H. Oberlies, Feras Q. Alali, and Shahab Uddin. "Anticancer Activity of Neosetophomone B, An Aquatic Fungal Secondary Metabolite, Against Hematological Malignancie S." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0106.
Full textDereli-Korkut, Zeynep, and Sihong Wang. "Microfluidic Cell Arrays to Mimic 3D Tissue Microenvironment." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80411.
Full textBaust, John M., Robert G. Van Buskirk, and John G. Baust. "Cryopreservation of an Engineered Skin Equivalent: The Apoptosis Paradigm." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0586.
Full textТрушина, Элеонора Николаевна. "APOPTOSIS OF BRAIN NEURONS IN ISCHEMIA." In 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.
Full textLiu, Lei, Yingjie Zhang, and Xianwang Wang. "Involvement of caspase-dependent and -independent apoptotic pathways in cisplatin-induced apoptosis." In SPIE BiOS: Biomedical Optics, edited by Wei R. Chen. SPIE, 2009. http://dx.doi.org/10.1117/12.808431.
Full textCheng, Chao-Min, and Philip R. LeDuc. "Effects of Local Mechanical Stimulation on Cellular Behavior." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176082.
Full text"APOPTOSIS AND ASSESSMENT OF CYTOGENETIC DISORDERS APOPTOSIS AND ASSESSMENT OF CYTOGENETIC DISORDERS IN THE POPULATION OF THE ARCTIC ZONE OF THE RUSSIAN FEDERATION." In 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.
Full textKessel, David, Yu Luo, and Hyeong-Reh C. Kim. "Determinants of PDT-induced apoptosis." In BiOS 2000 The International Symposium on Biomedical Optics, edited by Thomas J. Dougherty. SPIE, 2000. http://dx.doi.org/10.1117/12.379884.
Full textReports on the topic "Apoptosis"
Donato, Nicholas J. Calcium-Mediated Apoptosis and Apoptotic Sensitization in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada418675.
Full textHolley, Christopher L. Reaper-Induced Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada411241.
Full textPerry, Jennifer. Reaper-Induced Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada462723.
Full textKornbluth, Sally A., and Erica K. Evans. Regulation of Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada381256.
Full textLiu, Junwei. Apoptosis-Dependent and Apoptosis-Independent Functions Bim in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada439201.
Full textMarcelli, Marco. Apoptosis in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2001. http://dx.doi.org/10.21236/ada398042.
Full textMarcelli, Marco. Apoptosis in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2002. http://dx.doi.org/10.21236/ada407231.
Full textVogel, Kristine S. Neurofibromin and Neuronal Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada429612.
Full textVogel, Kristine S. Neurofibromin and Neuronal Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada420881.
Full textZhang, Hong. A Novel Apoptosis Regulator. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada390571.
Full text