The homeobox gene Nkx2-5 is the earliest known marker of the cardiac lineage in vertebrate embryos. Nkx2-5 expression is first detected in mesodermal cells specified to form heart at embryonic day 7.5 in the mouse and expression is maintained throughout the developing and adult heart. In addition to the heart, Nkx2-5 is transiently expressed in the developing pharynx, thyroid and stomach. To investigate the mechanisms that initiate cardiac transcription during embryogenesis, we analyzed the Nkx2-5 upstream region for regulatory elements sufficient to direct expression of a lacZ transgene in the developing heart of transgenic mice. We describe a cardiac enhancer, located about 9 kilobases upstream of the Nkx2-5 gene, that fully recapitulates the expression pattern of the endogenous gene in cardiogenic precursor cells from the onset of cardiac lineage specification and throughout the linear and looping heart tube. Thereafter, as the atrial and ventricular chambers become demarcated, enhancer ...
We performed bio-ChIP-seq using streptavidin beads immunoprecipitation of biotinylated 5 cardiac transcription factors (fbio) and P300 antibody ChIP-seq. We used a dox-inducible dual adenovirus system to express biotinylated Core Cardiac TFs in HL1. One adenovirus expressed the dox-activated reverse tet activator protein (rtTA) and the E. coli biotinylating enzyme BirA from the cardiac specific rat troponin T promoter. The second virus expressed a Core Cardiac TF fused to a C-terminal flag-bio epitope tag, where bio is the 15 amino acid substrate for BirA. This in vivo biotinylation approach permits pulldown of different factors to be performed under identical, stringent conditions, and circumvents limitations posed by available antibodies. We titrated adenovirus and dox doses to express GATA4flbio and MEF2Aflbio at near endogenous levels. The same conditions were then used to express SRFflbio, TBX5flbio, and NKX2-5flbio. Reference: 12. de Boer E, Rodriguez P, Bonte E, Krijgsveld J, Katsantoni E ...
GATA4 has been ascribed to a number of critical functions in the heart, spanning from the specification and differentiation of cardiac myocytes early in development to the regulation of the cardiac hypertrophic response in the adult. GATA4 mediates these processes through the direct transcriptional control of key cardiac structural and regulatory genes.1 For example, GATA4 has been shown to directly bind the promoters of the ANF, BNP, α-MHC, and β-MHC genes, thereby controlling their expression in the heart.1 Indeed, 3 of these 4 genes showed altered expression in the hearts of Gata4fl/flβMHC-Cre mice, validating the previously proposed proximal regulatory role of GATA4. Cardiac-specific deletion of Gata4 also resulted in the dysregulation of approximately 1.0% of all cardiac-expressed genes, further supporting the overall importance of GATA4 as a homeostatic regulator of gene expression in the heart.. GATA4 is also thought to function as a critical regulator of cardiac hypertrophy, although ...
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Regulation of GATA1 gene expression by HIF1. (A) Real-time PCR analysis of HIF1A and GATA1 mRNA levels in K562 cells transfected with the HIF1α expression plas
GATA1 - Gata1 - Mouse, 4 unique 29mer shRNA constructs in retroviral untagged vector shRNA available for purchase from OriGene - Your Gene Company.
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Buy our Recombinant Human GATA3 protein. Ab114297 is a protein fragment produced in Wheat germ and has been validated in WB, ELISA, SDS-PAGE. Abcam provides…
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An advantage of the zebrafish model is that embryos can survive a cardiomyopathy, which facilitates the analysis of other phenotypes (Heicklen-Klein et al., 2005). In addition to the heart, we find that Gata4 is required for formation of the intestine, liver, pancreas and swim bladder. Gata4/Gata5/Gata6 gene expression has been previously associated with endoderm-derived organs, and mouse knockout models showed specific functions for Gata4 in the foregut (Kuo et al., 1997; Molkentin et al., 1997) and gastric (Jacobsen et al., 2002) epithelium, and for Gata6 in the visceral endoderm (Morrisey et al., 1998) and lung epithelium (Yang et al., 2002). The zebrafish gata5 gene is also essential for gut morphogenesis and liver development, based on the analysis of the faust mutant (Reiter et al., 1999; Reiter et al., 2001), and depletion of Gata6 in Xenopus or zebrafish endoderm appears to disrupt normal intestinal morphogenesis (Peterkin et al., 2003). Therefore, all three of these Gata genes have ...
The role of GATA‐6 in cardiogenesis to date has been unclear. Although gain‐of‐function experiments suggested a role for this GATA factor in heart formation (Jiang and Evans, 1996; Gove et al., 1997; Charron et al., 1999), some loss‐of‐function data suggested that it may not be required at all except in the absence of GATA‐4 and ‐5 (Jiang et al., 1998; Morrisey et al., 1998; Koutsourakis et al., 1999). However, antisense studies demonstrated a requirement for GATA‐6 for specific gene expression during the differentiation of rat neonatal cardiomyocytes in culture (Charron et al., 1999). In this study, we demonstrate for the first time a crucial requirement for GATA‐6 in the maturation and maintenance of cardiomyocytes during embryonic development. We have employed a loss‐of‐function model using antisense MOs to study the function of GATA‐6. The depletion of GATA‐6 in Xenopus and zebrafish embryos causes a dramatic loss of heart tissue. We found that maturation of the ...
GATA1 was first described as a transcription factor that activates the hemoglobin B gene in the red blood cell precursors of chickens.[30] Subsequent studies in mice and isolated human cells found that GATA1 stimulates the expression of genes that promote the maturation of precursor cells (e.g. erythroblasts) to red blood cells while silencing genes that cause these precursors to proliferate and thereby to self-renew.[31][32] GATA1 stimulates this maturation by, for example, inducing the expression of genes in erythroid cells that contribute to the formation of their cytoskeleton and that make enzymes necessary for the biosynthesis of hemoglobins and heme, the oxygen-carrying components of red blood cells. GATA1-inactivating mutations may thereby result in a failure to produce sufficient numbers of and/or fully functional red blood cells.[5] Also based on mouse and isolated human cell studies, GATA1 appears to play a similarly critical role in the maturation of platelets from their precursor ...
More than 30% of all human cancers contain activating mutations of the small G‐protein RAS. As a result of this, RAS has been intensely studied and many efforts have been made to identify pathways that sustain RAS‐driven transformation [1]. Recent studies have indicated that the transcription factor GATA2 is one of these partners in crime, but a mechanistic link between RAS and GATA2 had not been identified [2]. A paper in this issue of EMBO reports closes this gap showing that GATA2 can be activated by p38 in RAS‐transformed cells [3].. See also: KR Katsumara et al (September 2014) ...
Gene, Genes, Chromatin, Repression, Gene Expression, Transcription Factors, Transcription Factor, Association, DNA, Fog, Transcription Factor Gata1, Megakaryocytes, Erythroid Cells, Mice, Proteins, Regulation, Architecture, Cell Lineages, Mast Cells, Cell
Hematopoietic differentiation of the H1-GATA2−/− ES cell line. a CFUs of H1 or H1-GATA2−/− derived CD34+ cells. H1 or H1-GATA2−/− cells were co-cult
Introduction: GATA4 gene encodes a member of the GATA family of zinc-finger transcription factors. This protein is thought to regulate genes involved in...
This Is Article About Bokken, Katana Kayu, Tsuba Maru Gata Type 02 with Sageo (tali ito) Bokken dengan model Tsuba bentuk Moru Gata ini dilengkapi Sageo berwarna Hijau dan dilengkapi dengan ornamen-ornamen lainnya sehingga penampilannya mendekati kemiripan dengan pedang katana sungguhan. Disamping indah dipandang mata (cocok buat hiasan atau pajangan) juga sangat cocok untuk latihan seni beladiri samurai. Selain karena penampilannya yang indah, Sageo pada gagang… Selengkapnya ». Rating: 1.0 ...
The GATA1 gene is associated with X-linked GATA1-related cytopenia (MedGen UID: 335283) and X-linked Diamond-Blackfan anemia (MedGen UID: 266045).
Cardiac transcription factors orchestrate the complex cellular and molecular events required to produce a functioning heart. Misregulation of the cardiac transcription program leads to embryonic developmental defects and is associated with human congenital heart diseases. Recent studies have expanded our understanding of the regulation of cardiac gene expression at an additional layer, involving the coordination of epigenetic and transcriptional regulators. In this review, we highlight and discuss discoveries made possible by the genetic and embryological tools available in the zebrafish model organism, with a focus on the novel functions of cardiac transcription factors and epigenetic and transcriptional regulatory proteins during cardiogenesis ...
Zebrafish are capable of complete cardiac regeneration after resection of up to 20% of their apical myocardium or cryoinfarction throughout their whole life (Jopling et al, 2010). In contrast, mammals (the data are mainly from mice) can only effectively regenerate the heart during embryonic development or shortly after birth until P7, when myocyte proliferation ceases (Porrello et al, 2011). Indeed, the expression of cell cycle genes in the heart winds down within the first postnatal week, although transcriptional mechanisms of this phenomenon have remained elusive (Soonpaa et al, 1996). We demonstrated in this study that cardiac GATA4 becomes strongly downregulated at P7 and to a lesser extent also after cryoinjury in mice, whereas in zebrafish GATA4 expression is massively upregulated in cardiomyocytes in response to cardiac injury to enable regeneration.. GATA4 downregulation predisposes the neonatal mouse heart to defective regeneration as demonstrated by an increased scar size in the ...
Here, we report that a complex enhancer, encoded by the distant Tce1 activator of transcription factor Gata3, is necessary for T cell development and is critical for the generation of ETP and for CD4 development, as demonstrated by CRISPR/Cas-mediated genome editing. This analysis also illuminated the mechanism of action of Tce1 during T cell development and identified several transcription factors that are responsible for engaging this enhancer activity in T cells.. Many studies have shown that GATA3 is required at multiple stages for normal T cell development (1, 2). Its abundance varies significantly between stages and is tightly controlled (5-11, 74). Although several transcription factors have been proposed as upstream regulators of Gata3 by demonstration that they bind near the Gata3 1a and/or 1b promoters (39, 40, 50, 75, 76), a functional requirement for any of those binding sites has not been confirmed by in vivo mutagenesis. Furthermore, the data shown here and previously clearly ...
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Complete information for QRSL1 gene (Protein Coding), Glutaminyl-TRNA Synthase (Glutamine-Hydrolyzing)-Like 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
T GATA2 is present at larger levels within the endothelial cells comprising LVV leaflets (E, arrows) compared with endothelial cells lining the jugular veins and jugular lymph sacs (E, arrowheads). GATA2 can also be present in cardiac valves (F ) and arterial endothelial cells (J ). Boxed region...
Expression of GATA1 (ERYF1, GATA-1, GF1, NF-E1, NFE1) in liver tissue. Antibody staining with HPA000232, HPA000233 and CAB009195 in immunohistochemistry.
Expression of GATA1 (ERYF1, GATA-1, GF1, NF-E1, NFE1) in colon tissue. Antibody staining with HPA000232, HPA000233 and CAB009195 in immunohistochemistry.
GATA 3, 0.1 mg. The genes for all 4 subunits of the T-cell antigen receptor (alpha, beta, gamma and delta) are controlled by distinct enhancers and their enhancer-binding proteins.
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cdna:novel chromosome:VEGA66:14:63198922:63245271:-1 gene:OTTMUSG00000032593 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Gata4 description:GATA binding protein 4 ...
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I have had employment on my mind alot lately. I question whether or not I am ready to attempt a gradual return to work or if I should wait and speak with my MS doctor in October. I worry about my ability to do much of anything in my job that is waiting for me. I seem to have a number of options in the level of work I can choose to do at my job (so far, as set out by my employer) as well as the amount of pay I would receive (so far, as set out by my employer ...
Members of the GATA transcription factor family have been used in many transfection studies to investigate their roles in the regulation of gene expression. To correct for variations in transfection efficiency, the Renilla luciferase encoding plasmids pRL-TK and pRL-SV40 are commonly used as normalization controls. We report here that plasmids expressing GATA-4 or GATA-6 transcription factor increased Renilla luciferase gene expression by 2 to 8 fold when co-transfected with pRL-TK or pRL-SV40. This alteration of the control reporter gene activity was shown to cause erroneous normalization of transfection efficiency and thus misinterpretation of results in a transactivation assay. To circumvent the problem, we generated two mutant control plasmids from which putative GATA response elements were deleted. These deletions rendered pRL-SV40 unresponsive to GATA transcription factor stimulation and reduced the response of pRL-TK. A database search also indicates that consensus GATA binding sequences are
Ver más] GATA transcription factors are expressed in the mesoderm and endoderm during development. GATA1-3, but not GATA4, are critically involved in hematopoiesis. An enhancer (G2) of the mouse Gata4 gene directs its expression throughout the lateral mesoderm and the allantois, beginning at embryonic day 7.5, becoming restricted to the septum transversum by embryonic day 10.5, and disappearing by midgestation. We have studied the developmental fate of the G2-Gata4 cell lineage using a G2-Gata4Cre;R26REYFP mouse line. We found a substantial number of YFP+ hematopoietic cells of lymphoid, myeloid and erythroid lineages in embryos. Fetal CD41+ /cKit+ /CD34+ and Lin- /cKit+ /CD31+ YFP+ hematopoietic progenitors were much more abundant in the placenta than in the aorta-gonad-mesonephros area. They were clonogenic in the MethoCult assay and fully reconstituted hematopoiesis in myeloablated mice. YFP+ cells represented about 20% of the hematopoietic system of adult mice. Adult YFP+ hematopoietic stem ...
GATA4 and GATA6 play essential, but redundant, roles in pancreas formation in mice and GATA6 mutations cause pancreatic agenesis in humans. Recently, GATA6 mutations have also been linked to adult-onset diabetes with subclinical or no exocrine insufficiency suggesting an important role for GATA6 in human ß cell physiology. To investigate the role of GATA6 in adult endocrine pancreas, we generated mice in which Gata6 is specifically inactivated in the pancreas. These mice develop glucose intolerance. Islets deficient in GATA6 activity display decreased insulin content and impaired insulin secretion. Gata6-deficient ß cells exhibit ultrastructural abnormalities including increased immature insulin granules, swollen mitochondria and disorganized endoplasmic reticulum. We also demonstrate that Pdx1 expression in adult ß cells depends on GATA sites in transgenic reporter mice and loss of GATA6 greatly impacts ß cell specific gene expression. These findings demonstrate the essential role of GATA6 ...
Currently, volunteer donors serve as the primary source of platelets for transfusion. Donor-derived platelets have an extremely short shelf life, are not always available, and have potential to transmit infectious diseases to the recipient. Due to these limitations, induced pluripotent stem (iPS) cells and embryonic stem (ES) cells have been explored as renewable platelet sources for clinical applications. Platelets arise from megakaryocyte-erythroid progenitors (MEPs), and mutations in the gene encoding the transcription factor GATA1 lead to the MEP accumulation in both mice and humans. While GATA1-deficient murine ES cells can serve as a renewable source of MEPs in vitro, these progenitors do not fully mature into platelet-producing megakaryocytes following induced overexpression of GATA1. Ji-Yoon Noh and colleagues at the Childrens Hospital of Philadelphia developed a protocol that restores endogenous GATA1 levels in MEPs derived from murine ES cells in which Gata1 mRNA is inducibly targeted ...
Currently, volunteer donors serve as the primary source of platelets for transfusion. Donor-derived platelets have an extremely short shelf life, are not always available, and have potential to transmit infectious diseases to the recipient. Due to these limitations, induced pluripotent stem (iPS) cells and embryonic stem (ES) cells have been explored as renewable platelet sources for clinical applications. Platelets arise from megakaryocyte-erythroid progenitors (MEPs), and mutations in the gene encoding the transcription factor GATA1 lead to the MEP accumulation in both mice and humans. While GATA1-deficient murine ES cells can serve as a renewable source of MEPs in vitro, these progenitors do not fully mature into platelet-producing megakaryocytes following induced overexpression of GATA1. Ji-Yoon Noh and colleagues at the Childrens Hospital of Philadelphia developed a protocol that restores endogenous GATA1 levels in MEPs derived from murine ES cells in which Gata1 mRNA is inducibly targeted ...
MalaCards based summary : Gata1-Related X-Linked Cytopenia is related to dyserythropoietic anemia and thrombocytopenia and porphyria, congenital erythropoietic. An important gene associated with Gata1-Related X-Linked Cytopenia is GATA1 (GATA Binding Protein 1). Affiliated tissues include bone, bone marrow and myeloid ...
I did my PhD with Mark Ptashne, one of those molecular biologists I had read about in high school. I worked on basic mechanisms of transcription in yeast and mammals. Although this was a great time when we were trying to figure out how the black boxes of transcriptional activation (and repression) worked, I felt a need to explore these questions in a more biological context. So I went to Rosa Beddingtons laboratory. Rosa was a pioneer in early mouse development and she had just discovered a potential clue to how all mammals know how to distinguish between where to make their heads and tails. Work in her lab had uncovered a new anterior signaling centre in a little studied extra-embryonic endoderm lineage (visceral endoderm), previously thought to only play a support function in development. In Rosas lab in 1996, I needed an in vitro model that could be used for molecular biology that approximated the early embryo and extra-embryonic endoderm, and so I started working with ESCs. I honestly had ...
Pancreatic cancer is a highly lethal disease, characterized by early metastatic dissemination. Although a few recurrent genetic alterations have been identified and well characterized in pancreatic cancer patients, the molecular mechanisms underlying the progression to metastasis are still not well known. As a result, most patients succumb to the metastatic burden, rather than the primary tumor. One of the first step during the progression to invasive cancer is the conversion of epithelial cells to a more mesenchymal phenotype. This process is called epithelial-to-mesenchymal transition (EMT). We have described previously that the transcription factor GATA6 inhibits EMT in pancreatic cancer cells, thus functioning as a tumor suppressor in this context. Our aims are: 1. To identify new genes that are crucial for the metastatic conversion of pancreatic cancer, which might be of clinical use as molecular markers or therapeutic targets; 2. To dissect the function of known and novel EMT inducers and ...
GATA3 antibody for detecting human T-cell-specific transcription factor GATA-3. Validated on up to 12 cell lysates for western blotting. Try a trial size today.
GATA3 (phospho Ser308) antibody (GATA binding protein 3) for WB. Anti-GATA3 (phospho Ser308) pAb (GTX32396) is tested in Human, Mouse samples. 100% Ab-Assurance.
Affiliation:立教大学,理学部,教授, Research Field:Cell biology,Functional biochemistry,Cell biology, Keywords:ミトコンドリア,液胞型ATPase,オルガネラ,ATP,膜融合,組織特異的転写制御,GATA-GT1,品質管理,クロライドイオン,アポトーシス, # of Research Projects:21, # of Research Products:43, Ongoing Project:リン酸化修飾によるミトコンドリア機能と品質管理の制御機構
Breastfeeding can bring about many tricky issues for parents - and sometimes, you wouldnt even be aware of these challenges until youre facing them. We reveal ...
GATA transcription factors mediate cell differentiation in diverse tissues, and their dysfunction is associated with certain congenital human disorders. The six classical vertebrate GATA proteins, GATA-1 to GATA-6, are highly homologous, bear two tandem zinc fingers of the C(4) (GATA) type, and activate transcription. TRPS1, the only other vertebrate protein with the GATA motif, is a large, multitype zinc finger protein that harbors a single DNA-binding GATA domain and represses transcription. Monoallelic TRPS1 mutations cause two dominantly inherited human developmental disorders of the hair, face, and digits, tricho-rhino-phalangeal syndrome (TRPS) types I (MIM 190350) and III (MIM 190351); missense GATA domain mutations account for the more severe type III form. Here we report that heterozygous mice with deletions of the TRPS1 GATA domain (TRPS1(+/Deltagt)) display facial anomalies that overlap with findings for TRPS, whereas TRPS1(Deltagt/Deltagt) mice additionally reveal a complete
The tissue-restricted GATA-4 transcription factor and Nkx2-5 homeodomain protein are two early markers of precardiac cells. Both are essential for heart formation, but neither can initiate cardiogenesis. Overexpression of GATA-4 or Nkx2-5 enhances cardiac development in committed precursors, suggesting each interacts with a cardiac cofactor. We tested whether GATA-4 and Nkx2-5 are cofactors for each other by using transcription and binding assays with the cardiac atrial natriuretic factor (ANF) promoter_the only known target for Nkx2-5. Co-expression of GATA-4 and Nkx2-5 resulted in synergistic activation of the ANF promoter in heterologous cells. The synergy involves physical Nkx2-5-GATA-4 interaction, seen in vitro and in vivo, which maps to the C-terminal zinc finger of GATA-4 and a C-terminus extension; similarly, a C-terminally extended homeodomain of Nkx2-5 is required for GATA-4 binding. Structure/function studies suggest that binding of GATA-4 to the C-terminus autorepressive domain of ...
Children with Down syndrome (DS) up to the age of 4 years are at a 150-fold excess risk of developing myeloid leukemia (ML-DS). Approximately 4%-5% of newborns with DS develop transient myeloproliferative disorder (TMD). Blast cell structure and immunophenotype are similar in TMD and ML-DS. A mutation in the hematopoietic transcription factor GATA1 is present in almost all cases. Here, we show that simple techniques detect GATA1 mutations in the largest series of TMD (n = 134; 88%) and ML-DS (n = 103; 85%) cases tested. Furthermore, no significant difference in the mutational spectrum between the 2 disorders was seen. Thus, the type of GATA1 sequence mutation is not a reliable tool and is not prognostic of which patients with TMD are probable to develop ML-DS.
GATA3 has been identified as a master regulator of T helper cells, as well as being important for early thymic progenitors and T-cell commitment. However, Gata3 expression initiates already at the hematopoietic stem cell (HSC) level, implicating a potential role also in the regulation of HSCs. Herein we used a conditional Gata3 knockout strategy in which Gata3 expression was completely deleted from the earliest stage of embryonic hematopoietic development after emergence of HSCs from hemogenic endothelium. Through a detailed analysis of HSCs at the phenotypic and functional level, we demonstrate that steady-state levels of HSCs are normal in Gata3(fl/fl)Vav-Cre(tg/+) mice. Moreover, through long-term primary and secondary transplantation experiments, we also unequivocally demonstrate that Gata3 has a redundant role in post-transplantation HSC self-renewal.
Loss-of-function germline GATA2 mutations in patients with MDS/AML or MonoMAC syndrome and primary lymphedema reveal a key role for GATA2 in the lymphatic vasculature. Dec 2011 Kazenwadel J, Secker GA, Liu YJ, Rosenfeld JA, Wildin RS, Cuellar-Rodriguez J, Hsu AP, Dyack S, Fernandez CV, Chong CE, Babic M, Bardy PG, Shimamura A, Zhang M, Walsh T, Holland SM, Hickstein DD, Horwitz MS, Hahn CN, Scott HS, Harvey NL. Source Division of Haematology, Centre for Cancer Biology, SA Pathology, Adelaide, SA, Australia; Abstract Recent work has established that heterozygous germline GATA2 mutations predispose carriers to familial myelodysplastic syndrome (MDS)/acute myeloid leukaemia (AML), "MonoMAC" syndrome and DCML deficiency. Here, we describe a previously unreported MDS family carrying a missense mutation in GATA2 (p.Thr354Met), one patient with MDS/AML carrying a frameshift mutation in GATA2 (p.Leu332Thrfs*53), another individual with MDS harboring a GATA2 splice site mutation, and three patients ...
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