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  • 1
    Keywords: APOPTOSIS ; CELLS ; BLOOD ; CELL ; Germany ; IN-VIVO ; KINASE ; PATHWAY ; PATHWAYS ; SYSTEM ; DEATH ; PROTEIN ; PROTEINS ; RNA ; MICE ; NF-KAPPA-B ; ACTIVATION ; MECHANISM ; FAMILY ; primary ; INDUCTION ; T cell ; T cells ; T-CELL ; T-CELLS ; MEMBER ; MEMBERS ; TRANSGENIC MICE ; CD95 ligand ; CELL-DEATH ; INDUCED APOPTOSIS ; LYMPHOCYTES ; B-CELLS ; SIGNALING COMPLEX ; Bcl-2 ; molecular ; MOLECULAR-BASIS ; RE ; FAMILIES ; LIFE ; LEVEL ; cell death ; ANTIGEN RECEPTORS ; progenitor ; SUPPRESSOR ; FAS LIGAND ; AICD ; HEMATOPOIETIC PROGENITOR KINASE-1 ; USA ; B-LYMPHOCYTES ; FATE ; FRAGMENT ; FAMILY-MEMBER BIM ; B-CELL ; KINASE-1 ; EXPANSION ; caspase-3 ; block ; B cells ; BCL-2 FAMILY ; COMPLEMENT ; FULL-LENGTH ; MEDIATED CLEAVAGE ; SMALL INTERFERING RNA
    Abstract: Life and death of peripheral lymphocytes is strictly controlled to maintain physiologic levels of T and B cells. Activation-induced cell death (AICD) is one mechanism to delete superfluous lymphocytes by restimulation of their immunoreceptors and it depends partially on the CD95/CD95L system. Recently, we have shown that hematopoietic progenitor kinase 1 (HPK1) determines T-cell fate. While full-length HPK1 is essential for NF-KB activation in T cells, the C-terminal fragment of HPK1, HPK1-C, suppresses NF-KB and sensitizes toward AICD by a yet undefined cell death pathway. Here we show that upon IL-2-driven expansion of primary T cells, HPK1 is converted to HPK1-C by a caspase-3 activity below the threshold of apoptosis induction. HPK1-C selectively blocks induction of NF-kappa B-dependent antiapoptotic Bcl-2 family members but not of the proapoptotic Bcl-2 family member Bim.Interestingly, T and B lymphocytes from HPK1-C transgenic mice undergo AICD independently of the CD95/CD95L system but involving caspase-9. Knock down of HPK1/HPK1-C or Bim by small interfering RNA shows that CD95L-dependent and HPK1/HPK1-C-dependent cell death pathways complement each other in AICD of primary T cells. Our results define HPK1-C as a suppressor of antiapoptotic Bcl-2 proteins and provide a molecular basis for our understanding of CD95L-independent AICD of lymphocytes
    Type of Publication: Journal article published
    PubMed ID: 17712048
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  • 2
    Keywords: CELLS ; EXPRESSION ; CELL ; human ; INFORMATION ; SYSTEM ; SYSTEMS ; TOOL ; GENE-EXPRESSION ; GENOME ; RNA ; TISSUE ; TISSUES ; BIOLOGY ; MOLECULAR-BIOLOGY ; SEQUENCE ; SEQUENCES ; MATURATION ; TARGET ; IDENTIFICATION ; PATTERNS ; DIFFERENCE ; STABILITY ; Jun ; TARGETS ; FUTURE ; HEMATOPOIETIC-CELLS ; LOCATION ; POSTTRANSCRIPTIONAL REGULATION ; molecular biology ; molecular ; PATTERN ; LIBRARIES ; C-ELEGANS ; LINEAGE ; TRANSLATION ; analysis ; PROFILES ; EXPRESSION PROFILES ; rodents ; USA ; CAENORHABDITIS-ELEGANS/ ; UNIT ; PRECURSOR ; TOOLS ; SET ; MENTAL-RETARDATION PROTEIN ; MicroRNAs ; ZEBRAFISH ; MICRORNA ; miRNAs ; ANIMAL DEVELOPMENT
    Abstract: MicroRNAs (miRNAs) are small noncoding regulatory RNAs that reduce stability and/or translation of fully or partially sequence-complementary target mRNAs. In order to identify miRNAs and to assess their expression patterns, we sequenced over 250 small RNA libraries from 26 different organ systems and cell types of human and rodents that were enriched in neuronal as well as normal and malignant hematopoietic cells and tissues. We present expression profiles derived from clone count data and provide computational tools for their analysis. Unexpectedly, a relatively small set of miRNAs, many of which are ubiquitously expressed, account for most of the differences in miRNA profiles between cell lineages and tissues. This broad survey also provides detailed and accurate information about mature sequences, precursors, genome locations, maturation processes, inferred transcriptional units, and conservation patterns. We also propose a subclassification scheme for miRNAs for assisting future experimental and computational functional analyses
    Type of Publication: Journal article published
    PubMed ID: 17604727
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  • 3
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; proliferation ; BLOOD ; CELL ; KINASE ; PATHWAY ; PATHWAYS ; liver ; DISTINCT ; PROTEIN ; transcription ; MICE ; ACTIVATION ; DNA ; TRANSPLANTATION ; BINDING ; PROTEIN-KINASE ; SIGNAL ; DELETION ; FUSION ; DNA-BINDING ; SIGNALING PATHWAY ; STEM-CELLS ; CONSTITUTIVE ACTIVATION ; RECEPTORS ; HEMATOPOIETIC-CELLS ; ERYTHROPOIETIN ; STAT5A(-/-)5B(-/-) MICE ; C-KIT ; signaling ; HEMATOPOIESIS ; stem cells ; progenitor ; USA ; SELF-RENEWAL ; STEM ; MYELOPROLIFERATIVE DISORDERS ; TYROSINE KINASE JAK2 ; ERYTHROID PROGENITORS ; FETAL ; myeloid cells ; STEM-CELL-FACTOR ; STRESS ERYTHROPOIESIS
    Abstract: Erythropoiesis requires erythropoietin (Epo) and stem cell factor (SCF) signaling via their receptors EpoR and c-Kit. EpoR, like many other receptors involved in hematopoiesis, acts via the kinase Jak2. Deletion of EpoR or Janus kinase 2 (Jak2) causes embryonic lethality as a result of defective erythropoiesis. The contribution of distinct EpoR/Jak2-induced signaling pathways (mitogen-activated protein kinase, phosphatidylinositol 3-kinase, signal transducer and activator of transcription 5 [Stat5]) to functional erythropoiesis is incompletely understood. Here we demonstrate that expression of a constitutively activated Stat5a mutant (cS5) was sufficient to relieve the proliferation defect of Jak2(-/-) and EpoR(-/-) cells in an Epo-independent manner. In addition, tamoxifen-induced DNA binding of a Stat5a-estrogen receptor (ER)* fusion construct enabled erythropoiesis in the absence of Epo. Furthermore, c-Kit was able to enhance signaling through the Jak2-Stat5 axis, particularly in lymphoid and myeloid progenitors. Although abundance of hematopoietic stem cells was 2.5-fold reduced in Jak2(-/-) fetal livers, transplantation of Jak2(-/-)-cS5 fetal liver cells into irradiated mice gave rise to mature erythroid and myeloid cells of donor origin up to 6 months after transplantation. Cytokine-and c-Kit pathways do not function independently of each other in hematopoiesis but cooperate to attain full Jak2/Stat5 activation. In conclusion, activated Stat5 is a critical downstream effector of Jak2 in erythropolesis/myelopoiesis, and Jak2 functionally links cytokine- with c-Kit-receptor tyrosine kinase signaling
    Type of Publication: Journal article published
    PubMed ID: 18239084
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  • 4
    Keywords: CELLS ; INHIBITOR ; CELL ; Germany ; human ; INHIBITION ; SYSTEM ; ENZYMES ; GENE ; GENOME ; GENOME SEQUENCE ; PROTEIN ; CONTRAST ; SEQUENCE ; SEQUENCES ; chromosome ; VARIANTS ; SUBUNIT ; ACTIVE-SITE ; DESIGN ; DIFFERENCE ; Drosophila ; DROSOPHILA-MELANOGASTER ; ERYTHROCYTES ; ESCHERICHIA-COLI ; genome analysis ; GLUTATHIONE ; GLUTATHIONE-REDUCTASE ; INSECTICIDE RESISTANCE ; MELANOGASTER ; PHAGOCYTOSIS ; resistance ; SELENOCYSTEINE ; SINGLE-COPY ; VECTOR ; Plasmodium falciparum ; Anopheles gambiae ; Drosophila melanogaster ; Diptera ; insect redox metabolism
    Abstract: The mosquito, Anopheles gambiae, is an important vector of Plasmodium falciparum malaria. Full genome analysis revealed that, as in Drosophila melanogaster, the enzyme glutathione reductase is absent in A. gambiae and functionally substituted by the thioredoxin system. The key enzyme of this system is thioredoxin reductase-1, a homodimeric FAD-containing protein of 55.3 kDa per subunit, which catalyses the reaction NADPH + H+ + thioredoxin disulfide. NADP+ + thioredoxin dithiol. The A. gambiae trxr gene is located on chromosome X as a single copy; it represents three splice variants coding for two cytosolic and one mitochondrial variant. The predominant isoform, A. gambiae thioredoxin reductase-1, was recombinantly expressed in Escherichia coli and functionally compared with the wild-type enzyme isolated in a final yield of 1.4 U.ml(-1) of packed insect cells. In redox titrations, the substrate A. gambiae thioredoxin-1 (K-m = 8.5 muM, k(cat) = 15.4 s(-1) at pH 7.4 and 25degreesC) was unable to oxidize NADPH-reduced A. gambiae thioredoxin reductase-1 to the fully oxidized state. This indicates that, in contrast to other disulfide reductases, A. gambiae thioredoxin reductase-1 oscillates during catalysis between the four-electron reduced state and a two-electron reduced state. The thioredoxin reductases of the malaria system were compared. A. gambiae thioredoxin reductase-1 shares 52% and 45% sequence identity with its orthologues from humans and P. falciparum, respectively. A major difference among the three enzymes is the structure of the C-terminal redox centre, reflected in the varying resistance of catalytic intermediates to autoxidation. The relevant sequences of this centre are Thr-Cys-Cys-SerOH in A. gambiae thioredoxin reductase, Gly-Cys-selenocysteine-GlyOH in human thioredoxin reductase, and Cys-X-X-X-X-Cys-GlyOH in the P. falciparum enzyme. These differences offer an interesting approach to the design of species-specific inhibitors. Notably, A. gambiae thioredoxin reductase-1 is not a selenoenzyme but instead contains a highly unusual redoxactive Cys-Cys sequence
    Type of Publication: Journal article published
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  • 5
    Keywords: CANCER ; EXPRESSION ; CELL ; Germany ; GENE ; HYBRIDIZATION ; DNA ; INDEX ; tumour ; CONTRAST ; chromosome ; virus ; IN-SITU ; COMPARATIVE GENOMIC HYBRIDIZATION ; cytogenetics ; LYMPHOMA ; MALIGNANCIES ; NUMBER ; leukemia ; ABERRATIONS ; IN-SITU HYBRIDIZATION ; MORPHOLOGY ; ABNORMALITIES ; FLUORESCENCE ; IMBALANCES ; C-MYC ; INTERPHASE ; EPSTEIN-BARR-VIRUS ; B-CELL LYMPHOMA ; Bcl-2 ; chemoresistance ; F ; CHROMOSOMAL BREAKPOINTS ; Epstein-Barr virus ; FEATURES ; immunohistology ; molecular cytogenetics ; sporadic and endemic Burkitt's lymphoma ; TRANSLOCATIONS
    Abstract: The present study has compared immunohistological marker expression profiles and genomic imbalances in seven African endemic Burkitt's lymphomas (eBLs) with those in ten European B-cell lymphomas with MYC rearrangement as shown by fluorescence in situ hybridization (FISH) analysis. eBLs showed a typical histomorphology and a homogeneous immuno-profile: CD10+, CD38+, CD77+, bcl-2-, and IgM+. Epstein-Barr virus (EBV) DNA was present in all cases. On comparative genomic hybridization (CGH), only three out of six eBLs showed imbalances (median number of imbalances = 2), with gains on chromosome 17 in two eBLs. The European lymphomas were all highly proliferating, with a Ki-67 index of at least 90%, and included seven with morphology typical of sporadic Burkitt's lymphoma (sBL) and three immunoblastic diffuse large B-cell lymphomas with MYC rearrangement (MYC re+DLBCL). In contrast to eBL, the immuno-profiles of the European lymphomas were less homogeneous and inconsistent for CD10, CD38, CD77, IgM and bcl-2 expression. EBV DNA was not detected. In five of seven sBLs, CGH showed a higher number of imbalances (median = 6), with recurrent gains on chromosome 1q (3/7) and losses on 12q and 17p (2/7), whereas all three MYC re+DLBCLs had fewer imbalances (median = 4), with gains on 17q in two of three lymphomas. It is concluded that eBL has a homogeneous immunohistology and few secondary genomic aberrations, whereas MYC-rearranged and highly proliferating European B-cell lymphomas are a heterogeneous group that includes sBL and a subgroup of diffuse large B-cell lymphomas. Copyright (C) 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley Sons, Ltd
    Type of Publication: Journal article published
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  • 6
    Keywords: CANCER ; carcinoma ; CELL ; Germany ; LUNG ; PATHWAYS ; EXPOSURE ; RISK ; TISSUE ; radiation ; CIGARETTE-SMOKING ; SIGNAL-TRANSDUCTION ; adenocarcinoma ; squamous cell carcinoma ; PREVALENCE ; LUNG-CARCINOMA ; MATRIX ; radon ; INCREASE ; LEVEL ; lung carcinoma ; HISTOLOGY ; RADIATION EXPOSURE ; HEDGEHOG ; DAUGHTERS ; silicosis ; uranium mining
    Abstract: BACKGROUND. In East Germany, uranium mining was undertaken on a large scale from 1946 to 1990. Poor working conditions led to a high level of exposure to ionizing radiation and quartz dust. This analysis evaluates the histopathology of lung carcinoma ill uranium miners in relation to radon exposure and silicosis. METHODS. A database developed for autopsy cases ascertained in a pathological tissue repository, of German uranium miners was used to estimate odds ratios for developing lung carcinoma by major cell type with regard to radon exposure and silicosis. Silicosis information was extracted from autopsy protocols. Working level months (WLM) were calculated with a job-exposure matrix to assess lifetime radon exposure. Risk estimates were based oil 3414 male miners who died from small cell lung carcinoma (SCLC, n = 1446), squamous cell carcinoma (SqCC, n = 1006), or adenocarcinoma (AC, n = 962) between 1957 and 1990. RESULTS. SCLC and SqCC seem more likely to be associated with high radon exposure than AC. Mean Cumulative radon exposure was 868 (SD 631) WLM in SCLC, 871 (SD 652) WLM in SqCC, and 743 (SD 598) WLM in AC. Silicosis prevalence was 26% in SCLC 38% in SqCC, and 30% in AC. In silicotics, AC and SqCC had a relatively higher frequency at the expense of SCLC. SCLC occurred earlier than AC and SqCC. CONCLUSION. High radon exposure was associated with a higher relative frequency of SCLC and SqCC than AC. Silicosis tended to increase the appearance of SqCC and AC
    Type of Publication: Journal article published
    PubMed ID: 16411224
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  • 7
    Keywords: PEPTIDE ; CANCER ; CELLS ; BLOOD ; CELL ; CLINICAL-TRIAL ; COMBINATION ; NEW-YORK ; DISTINCT ; SAMPLE ; SAMPLES ; RESPONSES ; BASE ; CD8(+) T-CELLS ; T cell ; T cells ; T-CELL ; T-CELLS ; ASSOCIATION ; TRIAL ; TRIALS ; IDENTIFICATION ; ASSAY ; NUMBER ; CLINICAL-TRIALS ; COUNTRIES ; MELANOMA ; LYMPHOCYTES ; VARIABILITY ; PEPTIDES ; NETHERLANDS ; CD8(+) ; ELISPOT ; IMMUNOTHERAPY ; T-LYMPHOCYTES ; T lymphocyte ; sensitivity ; PERIPHERAL-BLOOD ; PROJECT ; INTERFERON-GAMMA ; tetramer ; T lymphocytes ; GUIDELINES ; HETEROGENEITY ; CANCER VACCINES ; ONCOLOGY ; monitoring ; INCREASE ; analysis ; methods ; ASSAYS ; PHASE ; technique ; USA ; RECOMMENDATIONS ; STANDARDIZATION ; VARIABLES ; immunology ; INCREASES ; clinical trial ; CELL RESPONSES ; IMPORTANT DETERMINANT ; CD4+T-CELL IMMUNITY ; CYTOKINE FLOW-CYTOMETRY ; GAMMA ELISPOT ASSAYS ; Interlaboratory testing
    Abstract: The interpretation of the results obtained from immunomonitoring of clinical trials is a difficult task due to the variety of methods and protocols available to detect vaccine-specific T-cell responses. This heterogeneity as well as the lack of standards has led to significant scepticism towards published results. In February 2005, a working group was therefore founded under the aegis of the Association for Immunotherapy of Cancer ("CIMT") in order to compare techniques and protocols applied for the enumeration of antigen-specific T-cell responses. Here we present the results from two consecutive phases of an international inter-laboratory testing project referred to as the "CIMT monitoring panel". A total of 13 centers from six European countries participated in the study in which pre-tested PBMC samples, synthetic peptides and PE-conjugated HLA-tetramers were prepared centrally and distributed to participants. All were asked to determine the number of antigen-specific T-cells in each sample using tetramer staining and one functional assay. The results of the first testing round revealed that the total number of cells analyzed was the most important determinant for the sensitive detection of antigen-specific CD8(+) T-cells by tetramer staining. Analysis by ELISPOT was influenced by a combination of cell number and a resting phase after thawing of peripheral blood mononuclear cells. Therefore, the experiments were repeated in a second phase but now the participants were asked to change their protocols according to the new guidelines distilled from the results of the first phase. The recommendations improved the number of antigen-specific T-cell responses that were detected and decreased the variability between the laboratories. We conclude that a two-step approach in inter-laboratory testing allows the identification of distinct variables that influence the sensitivity of different T-cell assays and to formally show that a defined correction to the protocols successfully increases the sensitivity and reduces the inter-center variability. Such "two-step" inter-laboratory projects could define rational bases for accepted international guidelines and thereby lead to the harmonization of the techniques used for immune monitoring
    Type of Publication: Journal article published
    PubMed ID: 17721783
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  • 8
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; CELL ; MORTALITY ; NEW-YORK ; DRUG ; HEART ; MICE ; PATIENT ; ACTIVATION ; MR ; NO ; UP-REGULATION ; CALCIUM ; FAILURE ; ANTAGONIST ; HEART-FAILURE ; NUCLEAR RECEPTORS ; USA ; corticosteroids ; aldosterone ; CA2+ CURRENT ; RAT CARDIOMYOCYTES ; calcium current
    Abstract: Despite the fact that mineralocorticoid receptor (MR) antagonist drugs such as spironolactone and eplerenone reduce the mortality in heart failure patients, there is, thus far, no unambiguous demonstration of a functional role of MR in cardiac cells. The aim of this work was to investigate the activation pathway(s) mediating corticosteroid-induced up-regulation of cardiac calcium current (I-Ca). In this study, using neonatal cardiomyocytes from MR or glucocorticoid receptor (GR) knockout (KO) mice, we show that MR is essential for corticosteroid-induced up-regulation of I-Ca. This study provides the first direct and unequivocal evidence for MR function in the heart
    Type of Publication: Journal article published
    PubMed ID: 18040710
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  • 9
    Keywords: CANCER ; carcinoma ; CELL ; Germany ; LUNG ; lung cancer ; LUNG-CANCER ; DISEASE ; EXPOSURE ; MORTALITY ; MECHANISM ; mechanisms ; SKIN ; ASSOCIATION ; DISTRIBUTIONS ; PATTERNS ; HEALTH ; smoking ; DATABASE ; STEM-CELLS ; SQUAMOUS-CELL CARCINOMA ; adenocarcinoma ; squamous cell carcinoma ; non-small cell lung cancer ; HETEROGENEITY ; CYTOKERATIN EXPRESSION ; LUNG-DISEASE ; MATRIX ; CELL CARCINOMA ; arsenic ; development ; HISTOLOGY ; USA ; PHOSPHATASE ; SQUAMOUS-CELL ; silicosis ; uranium mining ; PROPORTION ; CELL-LUNG-CANCER ; COPPER SMELTER ; HISTOLOGIC TYPES ; SMELTER WORKERS
    Abstract: The mechanisms of action of arsenic in the development of lung cancer are still not yet elucidated. Considering the relationship between arsenic and squamous cell carcinomas of the skin, we hypothesized that arsenic exposure may be more closely associated with squamous cell carcinoma of the lung. A comprehensive histopathological database and a detailed job-exposure matrix developed for former German uranium miners with exposure to arsenic, radon, and quartz were analyzed to quantitatively assess the effect of arsenic regarding cell type of lung cancer. The distributions of major lung cancer cell types in 1,786 German uranium miners were associated with levels of arsenic exposure under control for the other lung carcinogens. To evaluate the arsenic effects in association with a frequent occupational lung disease in miners stratification by silicosis was performed. There was an arsenic-related increase of the proportion of squamous cell carcinoma of the lung but restricted to miners without silicosis. The increase was found at all levels of co-exposure to radon and quartz dust. In miners with silicosis, the proportion of adenocarcinoma increased with rising arsenic exposure. Arsenic exposure was associated with non-small cell lung cancer. Silicosis turned out as major determinant of the cell type related with arsenic. These results indicate a cell type characteristic effect of arsenic in the development of lung cancer
    Type of Publication: Journal article published
    PubMed ID: 19020892
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  • 10
    Keywords: CELLS ; EXPRESSION ; CELL ; Germany ; human ; MICROSCOPY ; TOOL ; GENE ; PROTEIN ; PROTEINS ; DOMAIN ; TYPE-1 ; PARTICLES ; TRANSPORT ; virus ; FUSION ; DISPLAY ; TRAFFICKING ; DERIVATIVES ; ELECTRON ; WILD-TYPE ; PRODUCT ; HUMAN IMMUNODEFICIENCY VIRUS ; PLASMA-MEMBRANE ; MORPHOLOGY ; REPLICATION ; EPITOPE ; LIVE CELLS ; LIVING CELLS ; GAG ; VIRAL PROTEASE ; FLEXIBILITY ; CONSTRUCTION ; INFECTIVITY ; DYNAMIC PROCESSES ; NUCLEAR-LOCALIZATION ; GAG PROTEIN ; IMMUNODEFICIENCY-VIRUS ; protease ; EARLY STEPS ; electron microscopy ; HUMAN-IMMUNODEFICIENCY-VIRUS ; structural protein ; HIV-1 ; MATRIX ; PRODUCTS ; LIFE-CYCLE ; AXONAL-TRANSPORT ; NONDIVIDING CELLS ; VIRAL MATRIX PROTEIN
    Abstract: The introduction of a label which can be detected in living cells opens new possibilities for the direct analysis of dynamic processes in virus replication, such as the transport and assembly of structural proteins. Our aim was to generate a tool for the analysis of the trafficking of the main structural protein of human immunodeficiency virus type 1 (HIV-1), Gag, as well as for the analysis of virus-host cell interactions in an authentic setting. We describe here the construction and characterization of infectious HIV derivatives carrying a label within the Gag polyprotein. Based on our initial finding that a short epitope tag could be inserted near the C terminus of the matrix domain of Gag without affecting viral replication, we constructed HIV derivatives carrying the egfp gene at the analogous position, resulting in the expression of a Gag-EGFP fusion protein in the authentic viral context. Particles displaying normal viral protein compositions were released from transfected cells, and Gag-EGFP was efficiently processed by the viral protease, yielding the expected products. Furthermore, particles with mature morphology were observed by thin-section electron microscopy. The modified virus was even found to be infectious, albeit with reduced relative infectivity. By preparing mixed particles containing equimolar amounts of Gag-EGFP and Gag, we were able to obtain highly fluorescently labeled virion preparations which displayed normal morphology and full wild-type infectivity, demonstrating that the process of HIV particle assembly displays a remarkable flexibility. The fluorescent virus derivative is a useful tool for investigating the interaction of HIV with live cells
    Type of Publication: Journal article published
    PubMed ID: 15367647
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