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  • Articles  (22)
  • Mice  (19)
  • 30D50
  • rationality
  • Computer Science  (22)
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  • 1
    ISSN: 1572-9265
    Keywords: Primary ; 42C05 ; Secondary ; 30D50 ; 41A20 ; 41A55 ; Rational interpolation ; orthogonal functions ; Szegö theory ; Pick-Nevanlinna interpolation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Computer Science , Mathematics
    Notes: Abstract We shall consider nested spacesl n ,n = 0, 1, 21... of rational functions withn prescribed poles outside the unit disk of the complex plane. We study orthogonal basis functions of these spaces for a general positive measure on the unit circle. In the special case where all poles are placed at infinity,l n =∏ n , the polynomials of degree at mostn. Thus the present paper is a study of orthogonal rational functions, which generalize the orthogonal Szegö polynomials. In this paper we shall concentrate on the functions of the second kind which are natural generalizations of the corresponding polynomials.
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Numerical algorithms 21 (1999), S. 185-203 
    ISSN: 1572-9265
    Keywords: systems of differential equations ; analytic solutions ; matrix Padé approximation ; rationality ; minimum degrees ; uniqueness ; partial differential equations ; 41A21 ; 34A45 ; 35A35
    Source: Springer Online Journal Archives 1860-2000
    Topics: Computer Science , Mathematics
    Notes: Abstract In this paper we present a technique to study the existence of rational solutions for systems of differential equations — for an ordinary differential equation, in particular. The method is relatively straightforward; it is based on a rationality characterisation that involves matrix Padé approximants. It is important to note that, when the solution is rational, we use formal power series “without taking into account” their circle of convergence; at the end of this paper we justify this. We expound the theory for systems of linear first-order ordinary differential equations in the general case. However, the main ideas are applied in numerical resolution of partial differential equations.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Numerical algorithms 15 (1997), S. 167-192 
    ISSN: 1572-9265
    Keywords: Matrix Padé Approximation ; rationality ; minimum degrees ; uniqueness ; 65 ; 41 ; 15
    Source: Springer Online Journal Archives 1860-2000
    Topics: Computer Science , Mathematics
    Notes: Abstract In many applications it is of major interest to decide whether a given formal power series with matrix-valued coefficients of arbitrary dimensions results from a matrix-valued rational function. As the main result of this paper we provide an answer to this question in terms of Matrix Padé Approximants of the given power series. Furthermore, given a matrix rational function, the “smallest” degrees of the matrix polynomials which represent it are not necessarily unique. Therefore we study a certain minimality-type, that is, minimum degrees. We aim to obtain all the minimum degrees for the polynomials which represent the function as equivalents. In addition, given that the rational representation of the function for the same pair of degrees need not be unique, we have obtained conditions to study the uniqueness of said representation. All the results obtained are presented graphically in tables setting out the above information. They lead to a number of properties concerning special structures, staired blocks, in the Padé Table.
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  • 4
    Publication Date: 2002-05-04
    Description: Extracts of the resin of the guggul tree (Commiphora mukul) lower LDL (low-density lipoprotein) cholesterol levels in humans. The plant sterol guggulsterone [4,17(20)-pregnadiene-3,16-dione] is the active agent in this extract. We show that guggulsterone is a highly efficacious antagonist of the farnesoid X receptor (FXR), a nuclear hormone receptor that is activated by bile acids. Guggulsterone treatment decreases hepatic cholesterol in wild-type mice fed a high-cholesterol diet but is not effective in FXR-null mice. Thus, we propose that inhibition of FXR activation is the basis for the cholesterol-lowering activity of guggulsterone. Other natural products with specific biologic effects may modulate the activity of FXR or other relatively promiscuous nuclear hormone receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Urizar, Nancy L -- Liverman, Amy B -- Dodds, D'Nette T -- Silva, Frank Valentin -- Ordentlich, Peter -- Yan, Yingzhuo -- Gonzalez, Frank J -- Heyman, Richard A -- Mangelsdorf, David J -- Moore, David D -- New York, N.Y. -- Science. 2002 May 31;296(5573):1703-6. Epub 2002 May 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Caco-2 Cells ; Carrier Proteins/genetics/metabolism ; Cells, Cultured ; Chenodeoxycholic Acid/pharmacology ; Cholesterol/*metabolism ; Cholesterol, Dietary/administration & dosage ; DNA/metabolism ; DNA-Binding Proteins/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Hepatocytes/metabolism ; Histone Acetyltransferases ; Humans ; *Hydroxysteroid Dehydrogenases ; Hypolipidemic Agents/metabolism/*pharmacology ; Ligands ; Liver/metabolism ; *Membrane Glycoproteins ; Mice ; Nuclear Receptor Coactivator 1 ; Pregnenediones/metabolism/*pharmacology ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors/genetics/metabolism ; Receptors, Steroid/antagonists & inhibitors/metabolism ; Transcription Factors/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Transcriptional Activation/drug effects ; Transfection ; Tumor Cells, Cultured
    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
    Publication Date: 2006-07-29
    Description: Serotonin [5-hydroxytryptamine (5-HT)] neurotransmission in the central nervous system modulates depression and anxiety-related behaviors in humans and rodents, but the responsible downstream receptors remain poorly understood. We demonstrate that global disruption of 5-HT2A receptor (5HT2AR) signaling in mice reduces inhibition in conflict anxiety paradigms without affecting fear-conditioned and depression-related behaviors. Selective restoration of 5HT2AR signaling to the cortex normalized conflict anxiety behaviors. These findings indicate a specific role for cortical 5HT2AR function in the modulation of conflict anxiety, consistent with models of cortical, "top-down" influences on risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisstaub, Noelia V -- Zhou, Mingming -- Lira, Alena -- Lambe, Evelyn -- Gonzalez-Maeso, Javier -- Hornung, Jean-Pierre -- Sibille, Etienne -- Underwood, Mark -- Itohara, Shigeyoshi -- Dauer, William T -- Ansorge, Mark S -- Morelli, Emanuela -- Mann, J John -- Toth, Miklos -- Aghajanian, George -- Sealfon, Stuart C -- Hen, Rene -- Gingrich, Jay A -- KO8 MH01711/MH/NIMH NIH HHS/ -- P01 DA12923/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 28;313(5786):536-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Columbia University and the New York State Psychiatric Institute, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16873667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/*physiopathology ; Cerebral Cortex/*metabolism ; Conditioning (Psychology) ; Conflict (Psychology) ; Depression/physiopathology ; Exploratory Behavior ; Fear ; Limbic System/metabolism ; Mice ; Mice, Knockout ; Patch-Clamp Techniques ; Periaqueductal Gray/metabolism ; Prosencephalon/metabolism ; Receptor, Serotonin, 5-HT2A/genetics/*metabolism ; Receptor, Serotonin, 5-HT2C/metabolism ; Receptors, Neurotransmitter/metabolism ; Risk-Taking ; Serotonin/physiology ; *Signal Transduction ; Synaptic Transmission
    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: 2006-01-18
    Description: In the adult brain, neuroblasts born in the subventricular zone migrate from the walls of the lateral ventricles to the olfactory bulb. How do these cells orient over such a long distance and through complex territories? Here we show that neuroblast migration parallels cerebrospinal fluid (CSF) flow. Beating of ependymal cilia is required for normal CSF flow, concentration gradient formation of CSF guidance molecules, and directional migration of neuroblasts. Results suggest that polarized epithelial cells contribute important vectorial information for guidance of young, migrating neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sawamoto, Kazunobu -- Wichterle, Hynek -- Gonzalez-Perez, Oscar -- Cholfin, Jeremy A -- Yamada, Masayuki -- Spassky, Nathalie -- Murcia, Noel S -- Garcia-Verdugo, Jose Manuel -- Marin, Oscar -- Rubenstein, John L R -- Tessier-Lavigne, Marc -- Okano, Hideyuki -- Alvarez-Buylla, Arturo -- HD 32116/HD/NICHD NIH HHS/ -- NS 28478/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 3;311(5761):629-32. Epub 2006 Jan 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery and Developmental and Stem Cell Biology Program, University of California San Francisco, San Francisco, CA 94143, USA. sawamoto@sc.itc.keio.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16410488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Tissue Transplantation ; Cell Movement ; Cell Polarity ; Cerebral Ventricles/cytology/physiology ; Cerebrospinal Fluid/*physiology ; Choroid Plexus/secretion ; Cilia/physiology ; Ependyma/cytology/*physiology ; Epithelial Cells/physiology ; Intercellular Signaling Peptides and Proteins ; Mice ; Nerve Tissue Proteins/cerebrospinal fluid ; Neurons/cytology/*physiology ; Olfactory Bulb/cytology/physiology ; Recombinant Fusion Proteins/cerebrospinal fluid
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2010-08-14
    Description: Dendritic cells (DCs) play a vital role in initiating robust immunity against pathogens as well as maintaining immunological tolerance to self antigens. However, the intracellular signaling networks that program DCs to become tolerogenic remain unknown. We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells. Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease. Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732486/" 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/PMC3732486/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manicassamy, Santhakumar -- Reizis, Boris -- Ravindran, Rajesh -- Nakaya, Helder -- Salazar-Gonzalez, Rosa Maria -- Wang, Yi-Chong -- Pulendran, Bali -- HHSN266 200700006C/PHS HHS/ -- N01 AI50019/AI/NIAID NIH HHS/ -- N01 AI50025/AI/NIAID NIH HHS/ -- R01 AI048638/AI/NIAID NIH HHS/ -- R01 AI056499/AI/NIAID NIH HHS/ -- R01 DK057665/DK/NIDDK NIH HHS/ -- R01DK057665,/DK/NIDDK NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 DK057665/DK/NIDDK NIH HHS/ -- R37AI48638,/AI/NIAID NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19AI057266,/AI/NIAID NIH HHS/ -- U54 AI057157/AI/NIAID NIH HHS/ -- U54AI057157/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 13;329(5993):849-53. doi: 10.1126/science.1188510.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, and Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, GA 30329, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20705860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytokines/metabolism ; Dendritic Cells/*immunology/metabolism ; Gene Expression Profiling ; *Inflammation ; Inflammatory Bowel Diseases/*immunology ; Intestinal Mucosa/cytology/*immunology/metabolism ; Macrophages/immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; *Self Tolerance ; Signal Transduction ; T-Lymphocytes, Helper-Inducer/cytology/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Tretinoin/metabolism ; Wnt Proteins/metabolism ; beta Catenin/*metabolism
    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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  • 8
    Publication Date: 2011-03-26
    Description: Eosinophils are associated with helminth immunity and allergy, often in conjunction with alternatively activated macrophages (AAMs). Adipose tissue AAMs are necessary to maintain glucose homeostasis and are induced by the cytokine interleukin-4 (IL-4). Here, we show that eosinophils are the major IL-4-expressing cells in white adipose tissues of mice, and, in their absence, AAMs are greatly attenuated. Eosinophils migrate into adipose tissue by an integrin-dependent process and reconstitute AAMs through an IL-4- or IL-13-dependent process. Mice fed a high-fat diet develop increased body fat, impaired glucose tolerance, and insulin resistance in the absence of eosinophils, and helminth-induced adipose tissue eosinophilia enhances glucose tolerance. Our results suggest that eosinophils play an unexpected role in metabolic homeostasis through maintenance of adipose AAMs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144160/" 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/PMC3144160/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Davina -- Molofsky, Ari B -- Liang, Hong-Erh -- Ricardo-Gonzalez, Roberto R -- Jouihan, Hani A -- Bando, Jennifer K -- Chawla, Ajay -- Locksley, Richard M -- 5F30DK083194-02/DK/NIDDK NIH HHS/ -- AI026918/AI/NIAID NIH HHS/ -- DK063720/DK/NIDDK NIH HHS/ -- DP1 OD006415/OD/NIH HHS/ -- F30 DK083194-03/DK/NIDDK NIH HHS/ -- R01 AI030663/AI/NIAID NIH HHS/ -- R01 DK076760/DK/NIDDK NIH HHS/ -- R01 DK081405/DK/NIDDK NIH HHS/ -- R01 HL076746/HL/NHLBI NIH HHS/ -- R37 AI026918/AI/NIAID NIH HHS/ -- R37 AI026918-24/AI/NIAID NIH HHS/ -- T32 AI007290/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Apr 8;332(6026):243-7. doi: 10.1126/science.1201475. Epub 2011 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143-0795, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21436399" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Adipose Tissue, White/cytology/*immunology/*metabolism ; Animals ; Blood Glucose/*metabolism ; Cell Movement ; Dietary Fats/administration & dosage ; Eosinophilia/immunology ; Eosinophils/immunology/*physiology ; Glucose Intolerance ; Homeostasis ; Insulin/metabolism ; Insulin Resistance ; Interleukin-13/genetics/metabolism ; Interleukin-4/genetics/metabolism ; *Macrophage Activation ; Macrophages/*immunology/*metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Nippostrongylus ; Strongylida Infections/immunology/metabolism
    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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  • 9
    Publication Date: 2013-07-28
    Description: Gram-negative bacteria including Escherichia coli, Citrobacter rodentium, Salmonella typhimurium, and Shigella flexneri are sensed in an ill-defined manner by an intracellular inflammasome complex that activates caspase-11. We show that macrophages loaded with synthetic lipid A, E. coli lipopolysaccharide (LPS), or S. typhimurium LPS activate caspase-11 independently of the LPS receptor Toll-like receptor 4 (TLR4). Consistent with lipid A triggering the noncanonical inflammasome, LPS containing a divergent lipid A structure antagonized caspase-11 activation in response to E. coli LPS or Gram-negative bacteria. Moreover, LPS-mutant E. coli failed to activate caspase-11. Tlr4(-/-) mice primed with TLR3 agonist polyinosinic:polycytidylic acid [poly(I:C)] to induce pro-caspase-11 expression were as susceptible as wild-type mice were to sepsis induced by E. coli LPS. These data unveil a TLR4-independent mechanism for innate immune recognition of LPS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kayagaki, Nobuhiko -- Wong, Michael T -- Stowe, Irma B -- Ramani, Sree Ranjani -- Gonzalez, Lino C -- Akashi-Takamura, Sachiko -- Miyake, Kensuke -- Zhang, Juan -- Lee, Wyne P -- Muszynski, Artur -- Forsberg, Lennart S -- Carlson, Russell W -- Dixit, Vishva M -- New York, N.Y. -- Science. 2013 Sep 13;341(6151):1246-9. doi: 10.1126/science.1240248. Epub 2013 Jul 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA. kayagaki@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23887873" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspases/biosynthesis ; Cholera Toxin/immunology ; Disease Models, Animal ; Escherichia coli/immunology ; Escherichia coli Infections/genetics/immunology ; *Immunity, Innate ; Inflammasomes/*immunology ; Lipid A/genetics/*immunology ; Macrophages/*immunology ; Mice ; Mice, Mutant Strains ; Mutation ; Salmonella Infections/immunology ; Salmonella typhimurium/immunology ; Sepsis/immunology ; Toll-Like Receptor 4/*immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1997-10-24
    Description: BAD is a distant member of the Bcl-2 family that promotes cell death. Phosphorylation of BAD prevents this. BAD phosphorylation induced by interleukin-3 (IL-3) was inhibited by specific inhibitors of phosphoinositide 3-kinase (PI 3-kinase). Akt, a survival-promoting serine-threonine protein kinase, was activated by IL-3 in a PI 3-kinase-dependent manner. Active, but not inactive, forms of Akt were found to phosphorylate BAD in vivo and in vitro at the same residues that are phosphorylated in response to IL-3. Thus, the proapoptotic function of BAD is regulated by the PI 3-kinase-Akt pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉del Peso, L -- Gonzalez-Garcia, M -- Page, C -- Herrera, R -- Nunez, G -- CA-64556/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):687-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381178" target="_blank"〉PubMed〈/a〉
    Keywords: Androstadienes/pharmacology ; Animals ; Apoptosis ; Carrier Proteins/*metabolism ; Cell Line ; Chromones/pharmacology ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Humans ; Interleukin-3/*pharmacology ; Mice ; Morpholines/pharmacology ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; bcl-Associated Death Protein ; bcl-X Protein
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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