Search results

1

The role of genetic factors apoptosisi and 14-3-3 protein in the induction of some atopic diseases

100%

Jagiello E., Krasnowska M., Gacko M., Rucinska M., Skrzydlewski Z.

Postępy Higieny i Medycyny Doświadczalnej

|

1997

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vol. 51

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issue 4

385-398

EN

In this review we try to summarize some of the new informations about the genetic base of bronchial asthma. We also mention apoptosis (programmed cell death) as the process modulating cell proliferation, differentiation and death. According to the latest reports, the disorders of the regulation of apoptosis may play an important role an the pathogenesis of autoimmunologic and atopic diseases (including bronchial asthma), AIDS and neoplasmatic diseases. There is a linkage between the induction of apoptosis and signal transduction disorders. We describe the Raf/MECK/ERK/MAP signal transduction pathway and 14-3-3 protein - the peptide which possibly might participate in the initiation of the programmed cell death.

2

Rho kinase in the regulation of cell death and survival

80%

Shi J., Wei L.

|

2007

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vol. 55

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issue 2

61-75

EN

Rho kinase (ROCK) belongs to a family of serine/threonine kinases that are activated via interaction with Rho GTPases. ROCK is involved in a wide range of fundamental cellular functions, such as contraction, adhesion, migration, and proliferation. Recent studies have shown that ROCK plays an important role in the regulation of apoptosis in various cell types and animal disease models. Two ROCK isoforms, ROCK1 and ROCK2, are assumed to be function redundant, this based largely on kinase construct overexpression and chemical inhibitors (Y27632 and fasudil) which inhibit both ROCK1 and ROCK2. Gene targeting and RNA interference approaches allow further dissection of distinct cellular, physiological, and patho-physiological functions of the two ROCK isoforms. This review, based on recent molecular, cellular, and animal studies, focuses on the current understanding of ROCK signaling in the regulation of apoptosis and highlights new findings from recently generated ROCK-deficient mice.

3

Effect of structural modification at the 4, 3', and 2' positions of doxorubicin on topoisomerase II poisoning, apoptosis, and cytotoxicity in human melanoma cells

80%

Gruber B. M., Anuszewska E. L., Bubko I., Gozdzik A., Fokt I., Priebe W.

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2007

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vol. 55

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issue 3

193-198

EN

Introduction: The mechanism of the cytotoxicity of anthracyclines is pleiotropic and its significance in cell growth inhibition seems to be highly specific and dependent on cell type and anthracycline drug. Resistance and the high cardiotoxicity of anthracyclines have stimulated many studies aimed at identifying critical substituents required for optimal activity. Many authors point to the fact that the double-strand breaks, the consequence of the activity of topoisomerase II poisons, and the inability of cells to repair the DNA lesions are the signal for apoptosis. The aim of this study was to define the influence of 4-demetoxy 2'-halogenated analogs with altered basicity at the 3'-position on topoisomerase II and the relationship of that interaction with apoptosis and the cytotoxicity of these novel anthracyclines. Parental human ME18 melanoma cells and the ME18/R subline, obtained experimentally, resistant to doxorubicin (DOX), exposed to 1.7 and 8.6 muM DOX or its analogs, annamycin and WP903 (both 0.3 and 3.0 ?M) were studied. Materials and Methods: The MTT test was used to assay cytotoxicity. Interaction of the drugs with topoisomerase II and apoptosis were done by Western blot and fluorescence microscopy using Hoechst 33342. Results: The structural changes at positions 4, 2', and 3' can influence topoisomerase II interaction and apoptotic activity, although correlation between these events and cytotoxic consequences has not been proved. Conclusions: The biological response of the cells to the structurally similar anthracyclines may be variable and probably depends on the cell type which seems to be an additional problem in the multifactorial resistance of tumor cells to anthracyclines.

4

BH3-only proteins: the lords of death

80%

Fleischer A., Rebollo A., Ayllon V.

Archivum Immunologiae et Therapiae Experimentalis

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2003

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vol. 51

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issue 1

9-17

EN

Although the mechanisms by which Bcl-2 family proteins control the apoptotic machinery of the cell are not fully understood, it becomes clear that the role of BH3-only proteins consists in serving as sensors or sentinels of cellular damage, transducing the apoptotic stimuli to the mitochondria. For this reason, mammalian cells have developed several strategies for their strict regulation throughout evolution. This review aims to highlight the different ways by which BH3-only proteins are controlled, including transcriptional regulation, post-translational modifications and subcellular localization.

5

Dimerization, ROS formation, and biological activity of o-methoxyphenols

80%

Fujisawa S., Atsumi T., Murakami Y., Kadoma Y.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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vol. 53

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issue 1

28-38

EN

o-Methoxyphenols are antioxidants widely used in the cosmetic and food industries. Dimers from 1, 2, or 3 were synthesized and their radical-scavenging and biological activities were compared with those of the original or other phenols. Radical-scavenging was evaluated from a kinetic induction period method (IPM). To simulate biomimetic thiolcooxidation with antioxidants, the behavior of mixtures of 1, 2, 4, or catechin with mercaptomethylimidazole (MMI), a thiol was investigated using IPM. Polyphenols 4 and catechin was accompanied by extensive oxygen uptake, suggesting the formation of thiyl radicals from MMI and their reaction with molecular oxygen. In contrast, 1 markedly enhanced radical-scavenging without oxygen uptake, probably because of the formation of EUGQM/MMI-conjugates. 2 showed relatively small oxygen uptake, probably resulting from the predominant formation of benzyl radicals. Intracellular reactive oxygen species (ROS) in cancer cells by 4, but not by compounds 1, 2, 6, 7, 8, 9, and 10 was found, suggesting a possible link between physicochemical oxygen-uptake and intracellular ROS. The induction of apoptosis by 4 in HL-60 cells was accompanied by intracellular ROS. Dimers 6 and 7 inhibited nuclear factor (NF)-kappaB activation stimulated by lipopolysaccharide (LPS) in RAW 264.7 cells. Also, 6, 7, and 9 inhibited LPS-induced cyclooxygenase-2 expression in RAW 264.7 cells in a dose-dependent manner, whereas 1, 2 and 3 did not. Dimerization of o-methoxyphenols may be a useful tool for the design of drugs to act as potent chemopreventive and anticancer agents.

6

Toll-like receptors types 2 and 6 and the apoptotic process in human neutrophils

80%

Jablonska E., Marcinczyk M., Jablonski J.

Archivum Immunologiae et Therapiae Experimentalis

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2006

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vol. 54

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issue 2

137-142

EN

Introduction: Neutrophils (PMN) apoptosis plays an important role in limiting the last phase of inflammatory processes. It is unknown whether Toll-like receptor (TLR)2 acts independently or together with TLR6 in this process. Materials and Methods: The aim of this study was to estimate the relationship between the expressions of TLR2 and TLR6 and the apoptosis of human neutrophils in physiological conditions. We investigated the influence of recombinant human interleukin (IL)-18 and N-formyl-metionyl-leucyl-phenylalanine (fMLP) on the relationships between these receptors and neutrophil apoptosis. Results: Our results showed that after 4-h incubation, the percentage of apoptotic PMNs significantly increased compared with PMN counts before incubation. The stronger expression of TLR2 on the neutrophils suggests that this receptor contributes more significantly to the induction of PMN apoptosis than does TLR6. We also demonstrated an influence of recombinant human IL-18 (rhIL-18) on the expression of TLR6, whereas this effect was not observed in the expression of TLR2. We observed that both rhIL-18 and fMLP inhibited the apoptosis of PMNs and that rhIL-18 had a stronger effect than fMLP. Conclusions: The obtained results suggest that not only TLR2, but also TLR6 plays an important role in the regulation of the apoptosis of PMNs. Changes in the expression of TLR6 and inhibition of apoptosis of PMNs by rhIL-18 seem to confirm the vital role this receptor and of rhIL-18 in regulating the survival of these cells. These data can be useful in developing methods to regulate PMN apoptosis in conditions associated with their excessive and unfavorable activation.

7

Erythropoietin preconditioning suppresses neuronal death following status epilepticus in rats

80%

Yang J., Huang Y., Yu X., Sun H., Li Y., Deng Y.

Acta Neurobiologiae Experimentalis

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2007

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vol. 67

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issue 2

141-148

EN

Status epilepticus (SE) is a grave condition in which the brain undergoes lasting seizures which can lead to neuronal loss. Our previous study suggested that preconditioning with erythropoietin (Epo) suppressed neuronal apoptosis in hippocampus of rats following SE in vivo by inhibiting caspase-3. In this study, we investigated the mechanisms by which Epo preconditioning may exert its anti-apoptotic effects using a lithium-pilocarpine induced SE model in rats. The effects of Epo on neuronal cell death were evaluated using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and the role of the Bcl-2 protein family, which have been shown to be anti- (Bcl-2, Bcl-w) or pro- (Bid, Bim) apoptotic, was examined with immunofluorescence. We found Epo preconditioning decreased the total number of TUNEL, Bim and Bid positive cells, but increased the total number of Bcl-w and Bcl-2 positive cells. These results suggest that systemic Epo pretreatment protects neurons in an acute phase of SE and may result in further suppression of neuronal apoptosis in hippocampus by regulating the balance between pro- and anti-apoptotic Bcl-2 family proteins.

8

Reactive oxygen intermediates and serum antioxidative system in patients with chronic C hepatitis treated with IFN-alpha and thymus factor X

80%

Jablonowska E., Tchorzewski H., Lewkowicz P., Kuydowicz J.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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vol. 53

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issue 6

529-533

EN

In this study, the chemiluminescence (CL) of peripheral blood polymorphonuclear leukocytes (PMNLs) and the serum total antioxidative system (TAS) were assessed in patients with chronic C hepatitis (CCH) before and after 3 and 6 months of treatment with interferon (IFN)- and thymus factor X (TFX). The study included 26 patients with CCH aged between 25?63 years (mean: 42.67). Combined therapy with IFN-alpha 2a and a TFX preparation was applied. PMNL metabolic activity was assessed applying the whole-blood CL method. We measured CL response of neutrophils unstimulated and stimulated by opsonized zymosan, N-formyl-methionyl-leucyl-phenylalanine (N-fMLP), and phorbol-myristate-acetate (PMA) without and after priming with tumor necrosis factor alpha (10 ng/ml). The assessment of serum TAS was performed directly before the beginning of therapy with IFN-alpha and TFX and after 3 and 6 months of the treatment. A colorimetric method based on the reduction of the cationic radical ABTS+ (cation 2, 2'-azido-bis-[3-ethylobenzothiazolino-6-sulfonate]) in the presence of serum antioxidants was used. As a result of the treatment with IFN-alpha and TFX, the formation of free oxygen radicals by resting (unprimed) neutrophils increased statistically significantly both without stimulation and following stimulation by fMLP and PMA. A statistically significant increase in the serum antioxidant capacity was observed, which suggests the induction of compensatory processes. Increased in vitro reactive oxygen species production by both stimulated and unstimulated peripheral blood neutrophils of patients with CCH was observed. Treatment with IFN-alpha and TFX resulted in a compensatory increase in serum antioxidative capacity.

9

Immunomodulation of macrophages by pathogenic Yersinia species

80%

Ruckdeschel K.

Archivum Immunologiae et Therapiae Experimentalis

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2002

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vol. 50

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issue 2

131-138

EN

The interaction between macrophages and bacterial pathogens plays a crucial role in the pathogenesis of infectious diseases. Pathogenic species of the gram-negative bacterium Yersinia deploy complex strategies to disarm macrophages and to disrupt their response to infection. For this purpose, Yersinia spp. engage a type III protein secretion system that mediates polarized translocation of Yersinia virulence factors, the so-called Yops, into the host cell cytoplasm. There, the Yops act on different cellular levels to neutralize a sequence of programmed phagocyte effector functions. Yersiniae initially impair the phagocytic machinery and block the generation of the bactericidal oxidative burst. Furthermore, yersiniae uncouple an array of fine-tuned signals of innate immunity, which leads to suppression of the macrophage TNF- production and to macrophage apoptosis. The impairment of cellular functions results in a scenario, by which Yersinia efficiently resist the attack of the macrophage and finally kills the macrophage by activating its intrinsic cell suicide mechanism. This review highlights the aspects of Yersinia-macrophage interaction that determine the fate of the infected cell.

10

Bcl-2 proteins in ovarian apoptosis

80%

Opiela J., Katska-Ksiazkiewicz L.

Biotechnologia

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2006

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issue 1

90-96

EN

Members of the Bcl-2 family are considered principal players in the cascade of events that activate or inhibit apoptosis. Recent evidence strongly supports fundamental role of Bcl-2 and related proteins in regulating ovarian cell death. This article will provide an overview of the current knowledge regarding Bcl-2 proteins in programmed cell death in development of the ovary and the postnatal ovarian cycles.

11

Apoptosis-the programmed cell death

80%

Gora-Tybor J., Robak T.

Postępy Higieny i Medycyny Doświadczalnej

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1994

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vol. 48

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issue 3

209-225

EN

Apoptosis is structurally distinct programmed cell death pathway.It takes place during embryogenesis, after withdrawal of the trophic hormones and in the course of normal tissue turnover.Defective regulation of apoptosis may play a very important role in the aetiology of cancer and other diseases.In this paper these and other problems concerning with apoptosis are reviewed.

12

The intestinal trefoil factor (Tff3), also expressed in the inner ear, interacts with peptides contributing to apoptosis

80%

Lubka M., Shah A. A., Blin N., Baus-Loncar M.

Journal of Applied Genetics

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2009

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vol. 50

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issue 2

167-171

EN

The 3 members of the mammalian trefoil factor family (TFF) are expressed and secreted as cytoprotective peptides along the entire length of the normal gastrointestinal tract. More recently, they were shown to display multifunctional properties. Goblet cells of the small and large intestine constitute a major source for the synthesis of the third family member, TFF3 (formerly intestinal trefoil factor, ITF). TFF3, like the other family members, is rapidly up-regulated in response to physical wounding of the digestive tract. In addition, Tff3 was also detected in the posterior pituitary gland. Apart from this Tff3 function as a neuropeptide, also presence of Tff3 in the mouse cochlea was noted and Tff3-deficient animals display hearing impairment and accelerated presbyacusis. To elucidate Tff3's mode of function and its unexpected contribution to the hearing process, we strived to determine Tff3's interacting partners and to establish the functional network. To this end, we used a protein-protein binding assay based on a specific transcriptional regulation in yeast cells (the yeast-two-hybrid assay). We looked for interacting partners of Tff3 in a mouse cochlea cDNA library (from donors aged 3?15 days, P3-P15). Our data show that several binding candidates exist and that they could contribute to the known involvement of the trefoil peptides to apoptosis.

13

Peroxisome proliferator-activated receptor gamma (PPARgamma) and sepsis

80%

von_ K. A., Soller M., Brune B.

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2007

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vol. 55

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issue 1

19-25

EN

This review describes the role of the nuclear hormone receptor PPARgamma as a double-edged sword in sepsis. On the one hand, PPARgamma inhibits pro-inflammatory gene expression, predominantly by scavenging transcription factors and their cofactors, thus preventing them from binding to their cognate binding sites in the promoters of target genes. The expressions of the affected genes, such as those for inducible nitric oxide synthase, TNF-alpha, or IL-1beta are repressed. Therefore, PPARgamma is suggested to be beneficial in hyper-inflammatory diseases, such as sepsis. In n animal models of sepsis, PPARgamma agonist pretreatment auspiciously attenuated inflammation compared with control animals, accompanied by their improved survival rate. On the other hand, PPARgamma provokes apoptosis, which in the hyper-inflammatory phase of sepsis might be helpful because the number of immune cells, such as monocytes, macrophages, and neutrophils, involved in secreting high amounts of pro-inflammatory mediators will be reduced. In contrast, during the anti-inflammatory phase, cell death of immune cells, especially of T lymphocytes, is supposed to be deleterious. Under these circumstances, a second infection cannot be adequately answered, thus causing septic shock and multi-organ dysfunction syndrome. Therefore the role of PPARgamma is still ambiguous. Particularly its role in initiating apoptosis awaits further clarification to finally elucidate its impact on sepsis development.

14

Apoptosis in oogenesis and preimplantation embryo development of mammals

80%

Warzych E., Lechniak D.

Biotechnologia

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2005

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issue 1

172-182

EN

In this paper, the authors made an attempt to summarize the present knowledge on apoptosis in mammalian oocytes and embryos. On the contrary to necrosis, apoptosis is a programmed death of damaged or mutated cells. Several studies showed that it takes place during oogenesis (oocyte growth and maturation), as well as at some stages of preimplantation embryo development (morula, blastocyst). Although apoptosis is observed in vivo, the frequency of this phenomenon increases in vitro. There is a number of methods detecting apoptotic cells, however, none of them gives a clear evaluation of the studied process. A complex analysis with the use of several methods is therefore advised. Because in ovary the majority of oocytes undergo atresia (over 99%), the scientists concentrate on developing new methods aiming at improvement of females' reproductive performance. The process of apoptosis seems to be a crucial limiting factor.

15

How do neurons degenerate in prion diseases or transmissible spongiform encephalopathies (TSEs): neuronal autophagy revisited

80%

Liberski P. P., Gajdusek D. C., Brown P.

Acta Neurobiologiae Experimentalis

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2002

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vol. 62

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issue 3

141-147

EN

As in other neurodegenerative diseases such as Alzheimer?s disease, neurons in prion diseases or transmissible spongiform encephalopathies (TSEs) die via programmed cell death of which the apoptotic process is relatively well characterized. A subcellular alteration linked to apoptosis is the formation of autophagic vacuoles, which we and others demonstrated in CJD- and scrapie-affected rodent brains. Autophagy may co-exist with apoptosis or may precede it and the process may be induced by apoptotic stimuli. Here, we extend these observations using different model of scrapie and CJD. Both scrapie models (the 263K and 22C-H) demonstrated autophagic vacuoles with the same frequency; hence, they will be described together. While the following changes had been observed simultaneously in different areas of the same sample, this description is organised as if it followed a sequence of events. First, a part of the neuronal cytoplasm was sequestrated by concentric arrays of membrane; that part of the cytoplasm closed by membranes appeared relatively normal but its density often appeared increased. Next, electron density of the central dramatically increased. Then, membranes proliferated within the cytoplasm in a labyrinth-like manner and an area sequestrated by these membranes enlarged and became more complex structure consisting of vacuoles, electron-dense area and areas of normally-looking cytoplasm connected with convoluted membranes. Finally, a large area of the cytoplasm was transformed into a collection of autophagic vacuoles of different sizes. Virtually identical alterations, albeit with much lower frequency, were seen in terminally ill CJD-affected hamsters.

16

TCR anti-H-Y/Db transgenic mice in studies on T-lymphocytes development and mechanisms of leukemogenesis

80%

Matuszyk J.

Postępy Higieny i Medycyny Doświadczalnej

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1995

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vol. 49

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issue 1

61-65

17

Apoptosis in human polymorphonuclear leukocytes: Searching for a genetic roadmap

80%

Kobayashi S. D., DeLeo F. R.

Archivum Immunologiae et Therapiae Experimentalis

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2003

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vol. 51

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issue 1

1-8

EN

Polymorphonuclear leukocytes (PMNs or neutrophils) are essential components of the innate immune system in humans and function primarily to eliminate invading microorganisms. Neutrophil influx to sites of infection is desirable because it also initiates an inflammatory response. Paradoxically, PMNs are also intimately associated with inflammatory disease. As part of normal neutrophil turnover in humans and to limit inflammatory potential, PMNs undergo programmed cell death or apoptosis. Several host factors, including cytokines and growth factors, are capable of extending neutrophil survival, and thus capacity to fight infection. On the other hand, phagocytosis of bacterial pathogens generally accelerates PMN apoptosis. Due in part to the extensive complexity of programmed cell death, relatively little is known about signaling pathways that govern these processes in PMNs. Recently, microarray strategies have been employed to gain an understanding of these processes in activated PMNs, and new evidence indicates that gene transcription is important in the regulation of neutrophil apoptosis and thus inflammation. A series of provocative discoveries led to the hypothesis that neutrophil programmed cell death is the result of an apoptosis differentiation program, a final stage of transcriptionally regulated PMN maturation or hematopoietic differentiation. Further characterization of the apoptosis differentiation program and associated biochemical pathways in mature PMNs will likely yield important insights into the resolution of inflammation and infection.

18

Modulation of apoptosis signaling for cancer therapy

80%

Fulda S., Debatin K.-M.

Archivum Immunologiae et Therapiae Experimentalis

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2006

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vol. 54

|

issue 3

173-175

EN

Apoptosis, the cell's intrinsic death program, plays a central role in regulating tissue homeostasis. Also, most cytotoxic therapies used for cancer treatment, such as chemotherapy, g-irradiation, suicide genes, or immunotherapy, predominantly act by triggering apoptosis in target cells. Thus, understanding the molecular events that regulate apoptosis and how tumor cells evade apoptotic deletion have provided a paradigm to link cancer genetics and response to cancer therapy. Therefore, insights into the mechanisms regulating drug-induced apoptosis provide rational targets for novel therapeutic interventions.

19

Components of the IFN- signaling pathway in tumorigenesis

80%

Blanck G.

Archivum Immunologiae et Therapiae Experimentalis

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2002

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vol. 50

|

issue 3

151-158

EN

Many features of the interferon (IFN-) signaling pathway would suggest that it is anti-tumorigenic. The IFN- signaling pathway leads to apoptosis and to the expression of immune function proteins that could cooperate with T cells in the destruction of tumor. Various lines of experimental approaches have in general supported the hypothesis the IFN- signaling pathway is anti-tumorigenic. However, data also indicate that the idea that the IFN- signaling pathway is exclusively anti-tumorigenic is too simplistic. Also, to date, very little of the knowledge regarding the anti-tumor effects of the IFN- pathway has been useful in the prognosis or therapy for cancer. This review summarizes the current state of knowledge regarding the IFN- signaling pathway in tumorigenesis, with an emphasis on MHC class II induction in tumor cells and the induction of apoptosis in tumor cells. The review also indicates some future areas of investigation that offer hope for applying this knowledge in reducing cancer mortality.

20

SEB-induced T cell apoptosis in atopic patients ? correlation to clinical status and skin colonization by Staphylococcus aureus

80%

Kedzierska A., Kaszuba-Zwoinska J., Slodowska-Hajduk Z., Kapinska-Mrowiecka M., Czubak M., Thor P., Wojcik K., Pryjma J.

Archivum Immunologiae et Therapiae Experimentalis

|

2005

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vol. 53

|

issue 1

63-70

EN

We asked whether in atopic dermatitis (AD) increased T cell apoptosis in staphylococcal enterotoxin B (SEB)-activated cultures of peripheral blood mononuclear cells (PBMCs) is characteristic of the exacerbation of the disease or connected with skin colonization by Staphylococcus aureus. The clinical status of the patients was evaluated using the SCORAD index. The number of bacteria colonizing patients' skin lesions was determined by the cfu method. Mononuclear cells isolated from peripheral blood were stimulated by SEB and the apoptosis of CD3+ cells in culture was determined by flow cytometry using the monoclonal antibody APO2.7. The cytokine production in the culture supernatants was determined by ELISA and Cytometric Bead Array kits. T cell apoptosis was increased, while the production of interferon (IFN)-? was reduced in cultures of PBMCs of AD patients during exacerbation. The proportion of CD3+APO2.7+ cells positively correlated with the density of S. aureus recovered from skin lesions, but not with SCORAD index. By contrast, SCORAD index, but not S. aureus density, negatively correlated with IFN-? production. Furthermore it was found that the presence of S. aureus on uninvolved skin distinguishes a group of severe cases with high serum IgE level, increased T cell apoptosis, and reduced production of tumor necrosis factor ? in SEB- -stimulated cultures. Among AD patients the increased activation-induced T cell apoptosis observed in SEB- -stimulated cultures is related to skin colonization by S. aureus. The presence of bacteria on uninvolved skin is a feature of a distinct group of AD patients.

Refine search results

The role of genetic factors apoptosisi and 14-3-3 protein in the induction of some atopic diseases

Rho kinase in the regulation of cell death and survival

Effect of structural modification at the 4, 3', and 2' positions of doxorubicin on topoisomerase II poisoning, apoptosis, and cytotoxicity in human melanoma cells

BH3-only proteins: the lords of death

Dimerization, ROS formation, and biological activity of o-methoxyphenols

Toll-like receptors types 2 and 6 and the apoptotic process in human neutrophils

Erythropoietin preconditioning suppresses neuronal death following status epilepticus in rats

Reactive oxygen intermediates and serum antioxidative system in patients with chronic C hepatitis treated with IFN-alpha and thymus factor X

Immunomodulation of macrophages by pathogenic Yersinia species

Bcl-2 proteins in ovarian apoptosis

Apoptosis-the programmed cell death

The intestinal trefoil factor (Tff3), also expressed in the inner ear, interacts with peptides contributing to apoptosis

Peroxisome proliferator-activated receptor gamma (PPARgamma) and sepsis

Apoptosis in oogenesis and preimplantation embryo development of mammals

How do neurons degenerate in prion diseases or transmissible spongiform encephalopathies (TSEs): neuronal autophagy revisited

TCR anti-H-Y/Db transgenic mice in studies on T-lymphocytes development and mechanisms of leukemogenesis

Apoptosis in human polymorphonuclear leukocytes: Searching for a genetic roadmap

Modulation of apoptosis signaling for cancer therapy

Components of the IFN- signaling pathway in tumorigenesis

SEB-induced T cell apoptosis in atopic patients ? correlation to clinical status and skin colonization by Staphylococcus aureus