Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.27.4 (ribonuclease)
 6,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The components of the insulin-like growth factor (IGF) axis have been investigated in the normal human thymus. Using ribonuclease protection assays (RPA), IGF-II transcripts were detected in the normal human thymus. By reverse transcriptase polymerase chain reaction (RT-PCR) analyses, promoters P3 and P4 were found to be active in the transcription of IGF2 gene within human thymic epithelial cells (TEC). No IGF-II mRNA could be detected in human lymphoid Jurkat T cells with 30 cycles of RT-PCR. By Northern blot analyses, IGFBP-2 to -6 (but not IGFBP-1) were found to be expressed in TEC with a predominance of IGFBP-4. Interestingly, Jurkat T cells only express IGFBP-2 but at high levels. The type 1 IGF receptor was detected in Jurkat T cells but not in human TEC. The identification of the components of the IGF axis within separate compartments of the human thymus adds further evidence for a role of this axis in the control of T-cell development. The precise influence of thymic IGF axis upon T-cell differentiation and immunological self-tolerance however needs to be further investigated.
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PMID:Characterization of the insulin-like growth factor axis in the human thymus. 1033 24

The human insulin-like growth factor-II (IGF2) is a regulatory peptide which is critical in normal fetal growth. IGF2 gene transcription is controlled by the usage of four promoters P1-P4 of which promoters P2-P4 are genomically imprinted. Disruption of imprinting and the resulting increase of gene dosage have been shown to be implicated in tumor progression in a variety of human tumors. Due to the need for high amounts of tissue material for conventional methods such as Northern blotting or ribonuclease protection assay (RPA), studies on IGF2 expression have most often been limited to the detection of total IGF2 transcript, though different dysregulatory events can be responsible for the abundance of IGF2 mRNA found in many tumors. We established a highly sensitive competitive RT-PCR assay for the four different transcripts of the IGF2 gene with transcript-specific external RNA competitors in which we take advantage of fluorescence-based quantification on a semiautomated sequencer. The amount of total RNA needed is approximately 100 times lower than the amounts required for Northern blotting or RPA, so that even cytological samples can be analyzed. We applied the assay to a series of eleven hepatoblastomas (HB) in which normal adjacent liver tissue could also be analyzed.
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PMID:Promoter-specific transcription of the IGF2 gene: a novel rapid, non-radioactive and highly sensitive protocol for mRNA analysis. 1178 54

A fluorescence-based method for simultaneously determining the diffusion coefficients of two proteins is described, and the diffusion coefficient of insulin-like growth factor (IGF-I) and ribonuclease (RNase) in a 0.27% fibrin hydrogel is reported. The method is based on two-color imaging of the relaxation of the protein concentration field with time and comparing the results with a transport model. The gel is confined in a thin (200 microm) capillary and the protein is labeled with a fluorescent dye. The experimentally determined diffusion coefficient of RNase (D = 1.21 x 10(-6) cm(2)/s) agrees with literature values for dilute gels and bulk aqueous solutions, thus indicating the gel and the dye had a negligible effect on diffusion. The experimental diffusion coefficient of IGF-I (D = 1.59 x 10(-6) cm(2)/s), in the absence of binding to the fibrin matrix, is consistent with the dimensions of the molecule known from x-ray crystallography and a correlation between D and molecular weight based on 14 other proteins. The experimental method developed here holds promise for determining molecular transport properties of biomolecules under a variety of conditions, for example, when the molecule adsorbs to the gel or is convected through the gel by fluid transport.
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PMID:Diffusion of insulin-like growth factor-I and ribonuclease through fibrin gels. 1740 Jul 3

For significant improvements to occur in the survival of patients with idiopathic pulmonary fibrosis (IPF), it is necessary to develop novel and more precisely targeted therapies. The selection of future appropriate regimens must critically depend on improved characterization of the molecules driving the pathogenesis of IPF. It is well defined that IPF is characterized by the expression of genes indicating an active tissue remodeling program, including extracellular matrix (ECM) and basement membrane components, as well as myofibroblast-associated and epithelial cell-related genes. A few recent advances are worth mentioning. Pulmonary research demonstrates abnormal expression of insulin-like growth factor (IGF) binding proteins (IGFBPs) in IPF, including human IPF bronchoalveolar lavage (BAL) cells and BAL fluids, human IPF fibroblasts, as well as fibrotic lung tissues of bleomycin-induced mice and IPF patients, analyzed by microarray, reverse transcription-polymerase chain reaction (RT-PCR), ribonuclease protection assay (RPA), Western blot, immunohistochemistry, or enzyme-linked immunosorbent assay (ELISA). Simultaneously, in vitro and in vivo studies indicate the involvement of IGFBPs in the initiation and development of the fibrosis process, including fibroblast activation and transdifferentiation to a myofibroblast phenotype, epithelial-mesenchymal transition (EMT), increased ECM production, and decreased ECM degradation, possibly contributing to the final lung fibrosis. These observations suggest that dysregulation of IGFBPs may be a key factor responsible for the initiation and perpetuation of IPF. Such efforts could lead to potential candidate molecules being exploited for therapeutic manipulation.
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PMID:Abnormal expression of IGF-binding proteins, an initiating event in idiopathic pulmonary fibrosis? 2045 31


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