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  • 1
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; IN-VITRO ; tumor ; CELL ; IN-VIVO ; MODEL ; MODELS ; PATHWAY ; PATHWAYS ; VITRO ; VIVO ; SYSTEM ; SYSTEMS ; DEATH ; GENE ; GENES ; microarray ; PROTEIN ; transcription ; EPITHELIA ; TUMORS ; validation ; MICE ; TRANSCRIPTION FACTOR ; KERATINOCYTES ; SKIN ; BIOLOGY ; cell cycle ; CELL-CYCLE ; CYCLE ; TARGET ; ISOFORM ; ENCODES ; PROMOTER ; PROMOTERS ; REQUIRES ; DNA-DAMAGE ; BAX ; HUMAN KERATINOCYTES ; SQUAMOUS-CELL CARCINOMA ; TARGETS ; RECEPTORS ; MICROARRAY ANALYSIS ; epidermis ; TRAIL ; DEATH RECEPTORS ; tetramer ; CD95 ; chemoresistance ; review ; TUMOR-SUPPRESSOR ; keratinocyte ; LIGHT ; TUMORIGENESIS ; development ; STRATIFIED EPITHELIA ; TARGET GENES ; analysis ; P63 ; death receptor ; EPITHELIUM ; EPITHELIAL TUMORS ; KINASE C-ABL ; P53-DEPENDENT APOPTOSIS ; REGULATES P73 ; USA ; function ; in vivo ; E ; PROTECTS ; MAINTENANCE ; inactive ; cornification ; FAMILY-MEMBER GENES ; GENE ENCODES ; IKK alpha ; ISOFORM EXPRESSION ; P53 HOMOLOG P63
    Abstract: The epidermis is a multilayered stratified epithelium, continuously regenerated by differentiating keratinocytes, that requires the transcription factor p63 for its development and maintenance. The TP63 gene encodes two major protein isoforms, TAp63 and Delta Np63, which have both transactivating and transcriptional repressing activities and regulate a wide range of target genes. TAp63 shows clear pro-apoptotic activity, mediated both by death receptors (CD95, TNF, TRAIL) and mitochondrial (bax, puma) pathways. Conversely, DNp63 protects from apoptosis by directly competing for TAp63 target promoters or sequestering it, forming inactive tetramers. Accordingly, p63 is expressed in epithelial tumors, contributing to both tumorigenesis and chemoresistance. However, the predominant physiological role of p63 is in epithelial development, as demonstrated by the lack of epidermis and other epithelia in p63-deficient mice. The specific role of TAp63 and DNp63 isoforms in epithelial development remains mostly unclear. Nevertheless, recent work utilizing in vivo genetic complementation of TAp63 and/or DNp63 into a p63 null background has shed new light into the specific functions of the two isoforms and allowed the in vivo validation of several p63 transcriptional targets, originally identified by microarray analysis in in vitro systems. However, despite concerted efforts to address the role of p63 isoforms, several questions remain unanswered. The main aim of this review is to critically discuss the data available in the literature and thoroughly analyze the models proposed
    Type of Publication: Journal article published
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  • 2
    Keywords: RECEPTOR ; APOPTOSIS ; EXPRESSION ; Germany ; PATHWAY ; SYSTEM ; SYSTEMS ; DEATH ; SITE ; GENE ; PROTEIN ; PROTEINS ; DIFFERENTIATION ; MONOCLONAL-ANTIBODY ; MECHANISM ; FAMILY ; INDUCTION ; mechanisms ; BINDING ; ALPHA ; CELL-DEATH ; PROMOTER ; p53 ; DNA-DAMAGE ; BAX ; MITOCHONDRIA ; RECEPTORS ; TRAIL ; Bcl-2 ; CD95 ; chemoresistance ; WILD-TYPE P53 ; signaling ; chemosensitivity ; CLINICAL-RELEVANCE ; CHEMOTHERAPEUTIC DRUGS ; INDUCE ; P63 ; death receptor ; BCL-2 FAMILY MEMBERS ; BINDING-SITE ; KINASE C-ABL ; P53-DEPENDENT APOPTOSIS ; REGULATES P73 ; TAp63 ; TUMOR-SUPPRESSOR P53
    Abstract: TP63, an important epithelial developmental gene, has significant homology to p53. Unlike p53, the expression of p63 is regulated by two different promoters resulting in proteins with opposite functions: the full-length transcriptionally active TAp63 and the dominant-negative DNp63. We investigated the downstream mechanisms by which TAp63 alpha elicits apoptosis. TAp63 alpha directly transactivates the CD95 gene via the p53 binding site in the first intron resulting in upregulation of a functional CD95 death receptor. Stimulation and blocking experiments of the CD95, TNF-R and TRAIL-R death receptor systems revealed that TAp63a can trigger expression of each of these death receptors. Furthermore, our findings demonstrate a link between TAp63a and the mitochondrial apoptosis pathway. TAp63a upregulates expression of proapoptotic Bcl-2 family members like Bax and BCL2L11 and the expression of RAD9, DAP3 and APAF1. Of clinical relevance is the fact that TAp63a is induced by many chemotherapeutic drugs and that inhibiting TAp63 function leads to chemoresistance. Thus, beyond its importance in development and differentiation, we describe an important role for TAp63a in the induction of apoptosis and chemosensitivity
    Type of Publication: Journal article published
    PubMed ID: 15944736
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  • 3
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; EXPRESSION ; IN-VITRO ; tumor ; MODEL ; MODELS ; PATHWAY ; THERAPY ; VITRO ; DEATH ; GENE ; PROTEIN ; PROTEINS ; MECHANISM ; prognosis ; INDUCTION ; CONTRAST ; mechanisms ; TRANSCRIPTIONAL ACTIVITY ; PROMOTER ; STRESS ; p53 ; DNA-DAMAGE ; BAX ; Jun ; DEGRADATION ; INVOLVEMENT ; sensitivity ; CD95 ; neuroblastoma ; TUMOR-SUPPRESSOR ; BALANCE ; cell death ; DNA damage ; SUPPRESSOR ; P63 ; death receptor ; KINASE C-ABL ; DELTA-NP73 ; p73 ; PUMA ; scotin
    Abstract: p73, like its homologue, the tumor suppressor p53, is able to induce apoptosis in several cell types. This property is important for the involvement of p73 in cancer development and therapy. However, in contrast with p53, the TAp73 gene has two distinct promoters coding for two protein isoforms with opposite effects: while the transactivation proficient TAp73 shows pro-apoptotic effects, the amino-terminal-deleted &UDelta; Np73 has an anti-apoptotic function. Indeed, the relative expression of these two proteins is related to the prognosis of several cancers. Here we discuss recent developments in the control of p73-induced apoptosis. First, TAp73 induces ER stress via the direct transactivation of Scotin. Second, TAp73 induces the mitochondrial pathway by directly transactivating both Bax and the BH3 only protein PUMA promoters. While the first transactivation is weak, and not sufficient to trigger apoptosis (at least in the in vitro cellular models so far evaluated), the induction of PUMA is strong and lethal. Third, the promoter of the death receptor CD95 contains a p53 responsive element and preliminary experiments suggest that TAp73 also activates the death receptor pathway. In addition, TAp73 is able to transactivate its own second promoter, thus inducing the expression of the antiapoptotic &UDelta; Np73 isoform. Therefore, the balance between TAp73 and &UDelta; Np73 finely regulates cellular sensitivity to death. © 2005 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15865927
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  • 4
    ISSN: 1095-8649
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: The reproductive biology of the Mediterranean razor fish Xyrichthys novacula was investigated by demographic data and histological analysis of the female, intersexual and male gonads. Specimens were collected by bottom trawl on a monthly basis between June 2000 and July 2001 in a sandy bay in southern Thyrrenian. Gonad histology confirmed that the Mediterranean razor fish is a monandric, protogynous hermaphrodite. Females reached first sexual maturity at 100 mm (LT) and the estimated mean LT at first maturity (L50) was 125 mm. Females exhibited asynchronous ovarian development and multiple ovulations occurred over the spawning period. Vitellogenesis started in early May and spawning occurred from late May until late September. Sexual transition involved a large-scale atresia of all oocyte stages and a massive degeneration of ovarian tissue followed by primordial germ cells proliferation. Sex change began at spawning time (June) but transitional individuals tended to cluster at the end of the reproductive period (September). They accounted for 17·1% of the population sampled and were found in a broad size range (105–150 mm LT).
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1095-8649
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: A histological analysis of the gonad of the pelagic crystal goby Crystallogobius linearis, from the coastal central area of the Adriatic Sea, showed it to be a truly semelparous species; after the first spawning the mature gonads of both males and females appeared to have lost the capability for further spawning. Mature females had very low fecundity (200–700 mature oocytes) and small egg size (0·2–0·55 mm) similarly to other progenetic species. This reproductive strategy is compared with that of Aphia minuta, and a possible cause for the post-reproductive mortality of the two gobies is suggested and discussed.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1095-8649
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Evidence is presented that apoptosis of intestinal enterocytes is implicated in adult mortality immediately after the breeding season in Aphia minuta, a paedomorphic goby that spends its whole life cycle of 〈1 year in the water column as a pelagic and planktophagous fish. This could be the first documented case in which apoptosis triggers a population dynamic process such as natural mortality in a vertebrate.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1095-8649
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: At variance with previous reports, the paedomorphic goby Aphia minuta does not show semelparity, but abbreviate iteroparity like other small Mediterranean gobiid species. In spring, the mature ovary contains several batches of eggs at different stages of vitellogenesis. This indicates that the breeding season of A. minuta is quite long and that spawning takes place at least twice during its short lifespan, involving in each ovulatory wave different batches of oocytes which undergo vitellogenesis at different times. These observations agree with the testicular cycle data. In males, which in spring exhibit active spermiation coinciding with deposition of the first batch of oocytes, spermatogonial mitosis also resumes, eventually resulting in the production of new sperm in summer.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1573-7373
    Keywords: IL-6 ; neuroblastoma ; melanoma ; retinoic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Preliminary data have shown that IL-6 may act as an autocrine growth factor to control proliferation. We further characterised the role of IL-6 in tumour growth as an autocrine/paracrine growth factor in neuroectodermal tumours. We evaluated the production and secretion of IL-6 by seven human melanoma, five neuroblastoma and one glioblastoma cell lines. Moreover, we determined their IL-6-dependent growth in serum free-medium or under minimal growth-supplement conditions: IL-6 dependent growth was observed in two non-IL-6 producing melanoma and in one neuroblastoma cell lines. In addition, expression of IL-6 mRNA and peptide was increased by retinoic acid. The data support the hypothesis that IL-6 contributes to neuroectodermal tumour growth, even though it shows a less potent effect than other reported growth factor such as IGF-II.
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  • 9
    ISSN: 1573-7373
    Keywords: neuroblastoma ; carbachol ; phosphoinositide hydrolysis ; calcium ; BAPTA/AM ; ionomycin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Stimulation of SK-N-BE(2) cells with 1 mM carbachol (Cch) elicited phosphoinositide (PPI) hydrolysis and a rapid elevation of cytosolic Ca2+ concentration ([Ca2+]i) from 115 nM to about 500 nM, followed by a plateau around 200 nM. In myo [3H]inositol-labelled cells, Cch-evoked accumulation of [3H]inositol phosphates (IPs) was not affected when [Ca2+]i was clamped at resting by cell loading with 10 μM BAPTA/AM; under these conditions, maximal 1,4,5-inositol trisphosphate accumulation was not reduced either. When [Ca2+]i was clamped around 700 nM by cell treatment with 600 nM ionomycin, Cch-evoked [3H]IPs accumulation was enhanced by less than 20%, but it was impaired by a 30% and a 55% after [Ca2+]i reduction to about 70 nM and 35—50 nM, by cell loading with 20 μM or 40 μM BAPTA/AM, respectively. These results show that, in SK-N-BE(2) cells, Cch-activated PPI-specific phospholipase C is sensitive to [Ca2+]i but it already operates under suboptimal conditions at resting [Ca2+]i.
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  • 10
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Central events in the host defence system and immune-mediated damage are tightly regulated by cell adhesion molecules. Sera from 28 human immunodeficiency virus (HIV)-1 infected children divided into groups according to disease severity, six seroreverting (SR) children and 25 healthy controls were studied to detect the presence of soluble intercellular adhesion molecule-1 (s-ICAM-1). Soluble ICAM-1 levels were found to be significantly increased in HIV-infected children in comparison with SR children or healthy controls. Levels of soluble ICAM-1 were higher in patients with severe forms of HIV-infection than in those with a milder form of the disease. Significant differences in titers of s-ICAM-1 were recorded between SR children and HIV-infected children with mild disease or healthy controls. There was a significant correlation between s-ICAM-1 levels and the concentrations of beta 2 microglobulin (β2m) and, to a lesser extend, immunoglobulin A levels (IgA). Soluble ICAM-1 levels didn't change considerably in HIV-infected children in stable clinical conditions, independently of their clinical stage of the disease, during a follow-up period of 9–12 months. Conversely, s-ICAM-1 levels increased simultaneously with the appearance of new well-defined clinical disorders or decreased during the improvement of clinical conditions. A significant negative correlation was recorded between the titers of the s-ICAM-1 and the CD4+ T-cell levels. These results suggest that the s-ICAM-1 might be another useful tool to evaluate disease progression.
    Type of Medium: Electronic Resource
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