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  • Germany  (12)
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  • 1
    Keywords: CELL ; Germany ; APOPTOSIS ; CELLS ; GROWTH ; PATHWAY ; PATHWAYS ; AP-1 ; ACTIVATION ; TIME ; MICE ; EFFICIENCY ; TOOL ; NEW-YORK ; INDUCTION ; T cells ; T-CELL ; T-CELLS ; T cell ; treatment ; SIGNAL ; c-Fos ; EAST ; c-Fos,apoptosis,early activation,induction,T cells ; GENOTYPES ; SIGNALING PATHWAY ; STIMULI ; WILD-TYPE ; SIGNALING PATHWAYS
    Abstract: We used c-Fos-deficient activated T cells from the spleen and c-Fos-deficient thymocytes to address the capacity of these cells to undergo apoptosis in response to various stimuli. To determine the role of c-Fos in apoptosis regulation in thymocytes, we challenged thymocytes from wild-type and c-Fos-deficient mice with either TPA or the glucocorticoid dexamethasone. After various time points cells were stained according to the Nicoletti method and analyzed by FACS. Thymocytes from both genotypes exhibited similar efficiency of apoptosis in response to treatment with TPA or dexamethasone. Our data provide clear evidence that c-Fos is not required for apoptosis regulation in activated T cells as well as in thymocytes
    Type of Publication: Book chapter
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  • 2
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; tumor ; carcinoma ; Germany ; human ; HYBRIDIZATION ; PROTEIN ; PROTEINS ; TISSUE ; TUMORS ; PATIENT ; FAMILY ; MARKER ; hormone ; IN-SITU ; PROGRESSION ; immunohistochemistry ; PATTERNS ; prostate cancer ; PROSTATE-CANCER ; MARKERS ; BENIGN ; GLYCATION END-PRODUCTS ; RAGE ; CARCINOMAS ; adenocarcinoma ; intraepithelial neoplasia ; NEURITE OUTGROWTH ; KAPPA-B ; CANCER PATIENTS ; HEALTHY ; prostate carcinoma ; OXIDANT STRESS ; SERUM ; in situ hybridization ; ELISA ; RE ; END ; TUMORIGENESIS ; HUMAN PROSTATE ; HYPERPLASIA ; TUMOR TISSUE ; MOLECULAR-GENETICS ; HUMAN-PROSTATE ; S100 PROTEINS ; EXPRESSION PATTERNS ; SERUM-LEVELS ; TUMOR DIFFERENTIATION
    Abstract: Purpose: S100 proteins comprise a family of calcium-modulated proteins that have recently been associated with epithelial tumors. We examined the expression of two members of this family, S10OA8 and S100A9, together with the S100 receptor RAGE (receptor for advanced glycation end products) in human prostate adenocarcinomas and in prostatic intraepithelial neoplasia. Experimental Design:Tissue specimens of 75 patients with organ-confined prostate cancer of different grades were analyzed by immunohistochemistry for expression of S10OA8, S100A9, and RAGE. In addition, in situ hybridization of S10OA8 and S10OA9 was done for 20 cases. An ELISA was applied to determine serum concentrations of S10OA9 in cancer patients compared with healthy controls or to patients with benign prostatic hyperplasia (BPH). Results: S100A8, S100A9, and RAGE were up-regulated in prostatic intraepithelial neoplasia and preferentially in high-grade adenocarcinomas, whereas benign tissue was negative or showed weak expression of the proteins. There was a high degree of overlap of S10OA8 and S10OA9 expression patterns and of S100A8 or S100A9 and RAGE, respectively. Frequently, a gradient within the tumor tissue with an increased expression toward the invaded stroma of the prostate was observed. S100A9 serum levels were significantly elevated in cancer patients compared with BPH patients or healthy individuals. Conclusion: Our data suggest that enhanced expression of S100A8, S100A9, and RAGE is an early event in prostate tumorigenesis and may contribute to development and progression or extension of prostate carcinomas. Furthermore, S100A9 in serum may serve as useful marker to discriminate between prostate cancer and BPH
    Type of Publication: Journal article published
    PubMed ID: 16033829
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  • 3
    Keywords: APOPTOSIS ; CANCER ; EXPRESSION ; GROWTH ; proliferation ; carcinoma ; CELL ; CELL-PROLIFERATION ; Germany ; LUNG ; DIAGNOSIS ; lung cancer ; LUNG-CANCER ; DEATH ; GENE ; GENES ; microarray ; PROTEIN ; cell line ; meningioma ; TISSUE ; LINES ; primary ; DOMAIN ; tumour ; SKIN ; BIOLOGY ; CELL-LINES ; MEMBER ; MOLECULAR-BIOLOGY ; SIGNAL ; PROGRESSION ; ASSAY ; INDUCED APOPTOSIS ; genetics ; COUNTRIES ; skin cancer ; CELL-LINE ; LINE ; ONCOGENE ; SUPERFAMILY ; EPITHELIAL-CELLS ; Jun ; PHENOTYPE ; STRATEGIES ; OVEREXPRESSION ; cell lines ; heredity ; LUNG-CARCINOMA ; SKIN-CANCER ; tumour suppressor gene ; ORIGIN ; molecular biology ; molecular ; ONCOLOGY ; non-small cell lung carcinoma ; SUPPRESSOR GENE ; cell proliferation ; SUPPRESSOR ; tumour suppressor ; NSCLC ; SET ; BREAST-CANCER CELLS ; DAL-1 ; ferm containing 3 ; GROWTH SUPPRESSION ; protein 4.1 ; PROTEIN 4.1B
    Abstract: Lung cancer including non-small cell lung carcinoma (NSCLC) represents a leading cause of cancer death in Western countries. Yet, understanding its pathobiology to improve early diagnosis and therapeutic strategies is still a major challenge of today's biomedical research. We analyzed a set of differentially regulated genes that were identifi. ed in skin cancer by a comprehensive microarray study, for their expression in NSCLC. We found that ferm domain containing protein 3 (FRMD3), a member of the protein 4.1 superfamily, is expressed in normal lung tissue but silenced in 54 out of 58 independent primary NSCLC tumours compared to patient-matched normal lung tissue. FRMD3 overexpression in different epithelial cell lines resulted in a decreased clonogenicity as measured by colony formation assay. Although cell attachment capabilities and cell proliferation rate remained unchanged, this phenotype was most likely owing to induced apoptosis. Our data identify FRMD3 as a novel putative tumour suppressor gene suggesting an important role in the origin and progression of lung cancer
    Type of Publication: Journal article published
    PubMed ID: 17260017
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  • 4
    Keywords: APOPTOSIS ; CELLS ; EXPRESSION ; Germany ; human ; SYSTEM ; DEATH ; SITE ; GENE ; GENE-EXPRESSION ; DRUG ; TISSUE ; NF-KAPPA-B ; LIGAND ; AP-1 ; primary ; INDUCTION ; T cells ; T-CELLS ; BINDING ; C-JUN ; SEQUENCE ; TRANSCRIPTION FACTORS ; ASSAY ; activation-induced cell death ; c-Fos ; CARCINOMA CELLS ; CD95 ligand ; CELL-DEATH ; CYCLOSPORINE-A ; FAS-LIGAND EXPRESSION ; INDUCED APOPTOSIS ; MOBILITY ; PROMOTER ; UP-REGULATION
    Abstract: The CD95 (APO-1/Fas) system plays a major role in induction of apoptosis in lymphoid and nonlymphoid tissues. The CD95 (APO- 1/Fas) ligand (CD95L) is induced in response to a variety of signals including TCR/CD3 stimulation or application of chemotherapeutic drugs. Here we report that an AP-1 site located in the 5' untranslated region of the CD95L gene is required for TCR/CD3-mediated induction of the human CD95L promoter. Electrophoretic mobility shift assays using nuclear extracts of Jurkat T cells as well as TCR/CD3-restimulated primary human T cells demonstrated specific binding of AP-1, predominantly composed of c-Jun and FosB, to this sequence. Ectopic expression of transdominant negative Jun mutants strongly reduced CD95L promoter activity and activation-induced cell death (AICD), confirming the functional significance of FosB/c-Jun binding. Thus, our results demonstrate an important novel function for FosB dimerized with c-Jun in TCR/CD3- mediated AICD in human T cells
    Type of Publication: Journal article published
    PubMed ID: 12618758
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  • 5
    Keywords: CELLS ; EXPRESSION ; CELL ; COMBINATION ; Germany ; human ; COHORT ; POPULATION ; RISK ; GENE ; PROTEIN ; SAMPLE ; SAMPLES ; DNA ; BINDING ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; HUMANS ; ASSAY ; PROMOTER ; SNP ; OBESITY ; SINGLE ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; FUNCTIONAL-CHARACTERIZATION ; HAPLOTYPES ; INSULIN-RESISTANCE ; metabolic syndrome ; USA ; REPLACEMENT ; Adiponectin ; STATE ; Luciferase reporter ; PLASMA ADIPONECTIN ; TYPE-2 DIABETIC-PATIENTS ; APM1 GENE ; HYPOADIPONECTINEMIA
    Abstract: OBJECTIVE-Adiponectin (APM1, ACDC) is an adipocyte-derived protein with downregulated expression in obesity and insulin-resistant states. Several potentially regulatory single nucleotide polymorphisms (SNPs) within the APM1 gene promoter region have been associated with circulating adiponectin levels. None of them have been functionally characterized in adiponectin-expressing cells. Hence, we investigated three SNPs (rs16861194, rs17300539, and rs266729) for their influence on adiponectin promoter activity and their association with circulating adiponectin levels. RESEARCH DESIGN AND METHODS-Basal and rosiglitazone-induced promoter activity of different SNP combinations (haplotypes) was analyzed in 3T3-L1 adipocytes using luciferase reporter gene assays and DNA binding studies comparing all possible APM1 haplotypes. This functional approach was complemented with analysis of epidemiological population-based data of 1,692 participants of the MONICA/KORA S123 cohort and 696 participants from the KORA S4 cohort for SNP and haplotype association with circulating adiponectin levels. RESULTS-Major to minor allele replacements of the three SNPs revealed significant effects on promoter activity in luciferase assays. Particularly, a minor variant in rs16861194 resulted in reduced basal and rosiglitazone-induced promoter activity and hypoadiponectinemia in the epidemiological datasets. The haplotype with the minor allele in all three SNPs showed a complete loss of promoter activity, and no subject carried this haplotype in either of the epidemiological samples (combined P value for statistically significant difference from a random sample was 0.006). CONCLUSIONS-Our results clearly demonstrate that promoter variants associated with hypoadiponectinemia in humans substantially affect adiponectin promoter activity in adipocytes. Our combination of functional experiments with epidemiological data overcomes the drawback of each approach alone. Diabetes 58-984-991, 2009
    Type of Publication: Journal article published
    PubMed ID: 19074982
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  • 6
    Keywords: CANCER ; CELLS ; EXPRESSION ; GROWTH ; SURVIVAL ; carcinoma ; CELL ; Germany ; human ; MODEL ; PATHWAY ; PATHWAYS ; NETWORK ; SUPPORT ; DEATH ; HEPATOCELLULAR-CARCINOMA ; liver ; GENE ; GENES ; PROTEIN ; PROTEINS ; TISSUE ; NF-KAPPA-B ; ACTIVATION ; murine ; CARCINOGENESIS ; INDUCTION ; SIGNAL ; TARGET ; MOUSE ; hepatocarcinogenesis ; hepatocellular carcinoma ; PROGRESSION ; CELL-DEATH ; CELL-LINE ; SIGNALING PATHWAY ; SIGNALING PATHWAYS ; RAGE ; MOUSE MODEL ; KAPPA-B ; OXIDATIVE STRESS ; expression profiling ; inflammation ; signaling ; MOLECULAR-MECHANISMS ; cell death ; CANCER PROGRESSION ; USA ; GROWTH-CONTROL ; SUPPRESSOR-CELLS ; nuclear factor kappa B ; COEXPRESSION ; COMPENSATORY PROLIFERATION
    Abstract: The nuclear factor-kappaB (NF-kappa B) signaling pathway has been recently shown to participate in inflammation-induced cancer progression. Here, we describe a detailed analysis of the NF-kappa B-dependent gene regulatory network in the well-established Mdr2 knockout mouse model of inflammation-associated liver carcinogenesis. Expression profiling of NF-kappa B-deficient and NF-kappa B-proficient hepatocellular carcinoma (HCC) revealed a comprehensive list of known and novel putative NF-kappa B target genes, including S100a8 and S100a9. We detected increased co-expression of S100A8 and S100A9 proteins in mouse HCC cells, in human HCC tissue, and in the HCC cell line Hep3B on ectopic RelA expression. Finally, we found a synergistic function for S100A8 and S100A9 in Hep3B cells resulting in a significant induction of reactive oxygen species (ROS), accompanied by enhanced cell survival. Conclusion: We identified S100A8 and S100A9 as novel NF-kappa B target genes in HCC cells during inflammation-associated liver carcinogenesis and provide experimental evidence that increased co-expression of both proteins supports malignant progression by activation of ROS-dependent signaling pathways and protection from cell death. (HEPATOLOGY 2009;50: 1251-1262.)
    Type of Publication: Journal article published
    PubMed ID: 19670424
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  • 7
    Keywords: CANCER ; CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; INHIBITOR ; tumor ; carcinoma ; Germany ; IN-VIVO ; VITRO ; GENE ; PROTEIN ; TUMORS ; MICE ; PATIENT ; FAMILY ; AP-1 ; CARCINOGENESIS ; INDUCTION ; KERATINOCYTES ; SKIN ; BINDING ; fibroblasts ; MOUSE ; c-Fos ; PROMOTER ; MOUSE SKIN ; TRANSFORMATION ; BENIGN ; CARCINOMAS ; squamous cell carcinoma ; GLUCOCORTICOID-RECEPTOR ; SKIN-CANCER ; BINDING PROTEIN ; keratinocyte ; TRANSITION ; MALIGNANT PROGRESSION ; INTERSTITIAL COLLAGENASE ; CELL-CARCINOMA ; dexamethasone ; MOUSE KERATINOCYTES ; RECYCLING ENDOSOMES
    Abstract: Malignant transformation of mouse skin by tumor promoters and chemical carcinogens, such as the phorhol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), is a multistage process leading to the formation of squamous cell carcinomas. it has been shown that mice lacking the AP-1 family member c-Fos exhibit an impaired transition from benign to malignant skin tumors. Here, we demonstrate enhanced expression of the small Ras-related GTPase Rab11a after short-term TPA treatment of mouse back skin. Expression of Rab11a in vivo and in vitro critically depended on c-Fos, because TPA application to the back skin of c-Fos-deficient mice and to mouse embryonic fibroblasts did not induce Rab11a mRNA or protein expression. Moreover, dexamethasone, which is a potent inhibitor of AP-1-mediated transactivation that exhibits anti-inflammatory and antitumor promoting activities, inhibited TPA-induced expression of Rab11a. Within the Rab11a gene promoter, we identified a functional AP-1 binding element that exhibited elevated c-Fos binding activity after TPA treatment of keratinocytes. Enhanced expression was not restricted to chemically induced mouse skin tumors but was also found in tumor specimens derived from patients with epithelial skin tumors. These data identify Rab11a as a novel, tumor-associated c-Fos/AP-1 target and may point to an as yet unrecognized function of Rab11a in the development of skin cancer
    Type of Publication: Journal article published
    PubMed ID: 15972968
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  • 8
    Keywords: APOPTOSIS ; CANCER ; EXPRESSION ; CELL ; Germany ; human ; IN-VIVO ; KINASE ; MODEL ; VIVO ; GENE ; GENE-EXPRESSION ; GENES ; HYBRIDIZATION ; PROTEIN ; RNA ; METABOLISM ; cell line ; LINES ; MICE ; DNA ; CARCINOGENESIS ; animals ; KERATINOCYTES ; SKIN ; BIOLOGY ; cell cycle ; CELL-CYCLE ; CELL-LINES ; CYCLE ; DOWN-REGULATION ; MOUSE ; IDENTIFICATION ; IN-SITU ; PROGRESSION ; MALIGNANCIES ; gene expression ; EXPRESSION ANALYSIS ; HUMANS ; DESIGN ; UP-REGULATION ; MOUSE SKIN ; skin carcinogenesis ; genetics ; statistics ; CELL-LINE ; LINE ; ADHESION ; CELL-ADHESION ; ONCOGENE ; INVOLVEMENT ; RT-PCR ; KINETICS ; cell lines ; heredity ; SKIN-CANCER ; HUMAN SKIN ; in situ hybridization ; MALIGNANCY ; ONCOLOGY ; ANNOTATION ; ENHANCED EXPRESSION ; cell adhesion ; LEVEL ; analysis ; CANCER DEVELOPMENT ; cluster analysis ; S100A8 ; MAP ; in vivo ; RELEVANCE ; Oligonucleotide Array Sequence Analysis ; SPECIMENS ; animal ; Carcinoma,Squamous Cell ; SQUAMOUS-CELL ; SET ; animal model ; molecular genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Skin Neoplasms ; Cell Line,Tumor ; cytology ; DNA,Complementary ; epithelial skin cancer ; Gene Expression Regulation,Neoplastic ; HUMAN-SKIN ; Microscopy,Fluorescence ; Protein-Serine-Threonine Kinases ; RNA,Messenger ; tumour specimen
    Abstract: Chemically induced mouse skin carcinogenesis represents the most extensively utilized animal model to unravel the multistage nature of tumour development and to design novel therapeutic concepts of human epithelial neoplasia. We combined this tumour model with comprehensive gene expression analysis and could identify a large set of novel tumour-associated genes that have not been associated with epithelial skin cancer development yet. Expression data of selected genes were confirmed by semiquantitative and quantitative RT-PCR as well as in situ hybridization and immunofluorescence analysis on mouse tumour sections. Enhanced expression of genes identified in our screen was also demonstrated in mouse keratinocyte cell lines that form tumours in vivo. Self-organizing map clustering was performed to identify different kinetics of gene expression and coregulation during skin cancer progression. Detailed analysis of differential expressed genes according to their functional annotation confirmed the involvement of several biological processes, such as regulation of cell cycle, apoptosis, extracellular proteolysis and cell adhesion, during skin malignancy. Finally, we detected high transcript levels of ANXA1, LCN2 and S100A8 as well as reduced levels for NDR2 protein in human skin tumour specimens demonstrating that tumour-associated genes identified in the chemically induced tumour model might be of great relevance for the understanding of human epithelial malignancies as well
    Type of Publication: Journal article published
    PubMed ID: 16247483
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  • 9
    Keywords: brain ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; INHIBITOR ; INVASION ; proliferation ; tumor ; CELL ; CELL-PROLIFERATION ; Germany ; human ; IN-VIVO ; MODEL ; VITRO ; VIVO ; GENE-EXPRESSION ; PROTEIN ; transcription ; cell line ; TISSUE ; TUMORS ; LINES ; MICE ; PATIENT ; TISSUES ; KERATINOCYTES ; SKIN ; T cell ; T-CELL ; CELL-LINES ; SIGNAL ; MOUSE ; STAGE ; UP-REGULATION ; MEMBRANE ; skin carcinogenesis ; CELL-LINE ; LINE ; ADHESION ; MIGRATION ; MORPHOLOGY ; INVOLVEMENT ; MOUSE MODEL ; TRANSLOCATION ; beta-catenin ; ECTODOMAIN ; cell lines ; SUBSTRATE-SPECIFICITY ; MATRIX ; E-cadherin ; ONCOLOGY ; RE ; CAPACITY ; keratinocyte ; cell proliferation ; LEVEL ; NUCLEAR ; USA ; TISSUE INHIBITOR ; cancer research ; in vivo ; PLASMID ; DEFECT ; PROMOTES ; matrix metalloproteinase ; METALLOPROTEINASE ; ectodomain shedding ; MATRIX-METALLOPROTEINASE ; OVARIAN-CARCINOMA ; GROWTH-CONTROL ; EXTRACELLULAR CLEAVAGE ; HUMAN TISSUE KALLIKREINS ; PROTEINASE-ACTIVATED RECEPTORS ; SERINE PROTEINASE ; SERUM BIOMARKER
    Abstract: Recently, we described phorbol ester-induced expression of the brain and skin serine proteinase Bssp/kallikrein 6 (Klk6), the mouse orthologue of human KLK6, in mouse back skin and in advanced tumor stages of a well-established multistage tumor model. Here, we show KLK6 up-regulation in squamous skin tumors of human patients and in tumors of other epithelial tissues. Ectopic Klk6 expression in mouse keratinocyte cell lines induces a spindle-like morphology associated with accelerated proliferation, migration, and invasion capacity. We found reduced E-cadherin protein levels in the cell membrane and nuclear translocation of beta-catenin in Klk6-expressing mouse keratinocytes and human HEK293 cells transfected with a KLK6 expression plasmid. Additionally, HEK293 cells exhibited induced T-cell factor-dependent transcription and impaired cell-cell adhesion in the presence of KLK6, which was accompanied by induced E-cadherin ectodomain shedding. Interestingly, tissue inhibitor of metalloproteinase (TIMP)-l and TIMP-3 interfere with KLK6-induced F-cadherin ectodomain shedding and rescue the cell-cell adhesion defect in vitro, suggesting the involvement of matrix metalloproteinase and/or a disintegrin and metalloproteinase (ADAM) proteolytic activity. In line with this assumption, we found increased levels of the mature 62-kDa ADAM10 proteinase in cells expressing ectopic KLK6 compared with mock controls. Finally, enhanced epidermal keratinocyte proliferation and migration in concert with decreased E-cadherin protein levels are confirmed in an in vivo Klk6 transgenic mouse model
    Type of Publication: Journal article published
    PubMed ID: 17804733
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  • 10
    Keywords: CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; proliferation ; CELL ; Germany ; VITRO ; transcription ; TISSUE ; LINES ; MICE ; FAMILY ; TRANSCRIPTION FACTOR ; AP-1 ; TISSUES ; cell cycle ; CELL-CYCLE ; CYCLE ; MEMBER ; SIGNAL ; bone marrow ; BONE-MARROW ; TRANSGENIC MICE ; c-Fos ; NUMBER ; transgenic ; LINE ; MUTANT MICE ; ACTIVATING TRANSCRIPTION FACTOR-2 ; AP-1,bone,chondrocytes,cell cycle,osteoblasts,osteoporosis ; BONE-FORMATION ; EMBRYONIC LETHALITY ; GROWTH-PLATE CHONDROCYTES ; HERITABLE DISEASES ; LINEAGE DETERMINATION ; MOLECULAR INSIGHTS ; NATRIURETIC PEPTIDE ; OSTEOBLAST-LIKE CELLS ; OSTEOPOROSIS ; REGULATOR ; REGULATORS ; SKELETAL DEVELOPMENT
    Abstract: Functional analysis in mice has established an absolute requirement of JunB, a member of the AP-1 transcription factor family, during early embryonic development. To investigate the role of JunB during mid and late gestation and postnatally Ubi-junB transgenic mice were used to generate two junB(-/-) Ubi-junB mutant lines, in which embryonic lethality was rescued but strongly reduced JunB; expression in several adult tissues was observed. Mutant mice from both rescue lines were growth retarded and shared significantly reduced longitudinal bone growth. Mutant long bones were characterised by reduced numbers of growth plate chondrocytes and a severe osteoporosis. Decreased JunB levels in epiphysal growth plate chondrocytes and bone lining osteoblasts correlated with deregulated expression of Cyclin A, Cyclin D1 and p16(INK4a), key regulators of cell cycle control. Furthermore, junB(-/-) Ubi-junB bone marrow stromal cells were unable to differentiate into bone forming osteoblasts in vitro. Our data demonstrate that JunB plays a crucial role in endochondral ossification by regulating proliferation and function of chondrocytes and osteoblasts
    Type of Publication: Journal article published
    PubMed ID: 14576352
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