Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.23.5 (cathepsin D)
4,130 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunohistochemical studies were carried out on the new type of cerebral cortical astrocytic inclusions recently discovered in a 20-year-old patient with maldeveloped brain and micropolygyria. The inclusions appeared as eosinophilic structures (hematoxylin and eosin stain) and did not exhibit argyrophilia (modified Bielschowsky method). The inclusions were strongly stained by the antibody against S-100 protein (S 100) and to a lesser extent by the antibody to microtubule-associated protein 1B (MAP 1B). In contrast to Rosenthal fibers, the astrocytic inclusions did not react with antibodies to alpha B-crystallin, glial fibrillary acidic protein and ubiquitin. No positive reactions were obtained with antibodies against heat-shock protein 27 (HSP 27), HSP 72, actin, vimentin, desmin, cytokeratin, myelin basic protein, beta-tubulin, MAP 2, tau protein, paired helical filament, phosphorylated neurofilament protein (NFP), nonphosphorylated NFP, synaptophysin, cathepsin D, alpha 1-antichymotrypsin, alpha 1-antitrypsin and basic fibroblast growth factor. By immunoelectron microscopy, the products of the reaction with the anti-S 100 antibody appeared as heterogeneous granular deposits and with the antibody to MAP 1B they were randomly scattered throughout the astrocytic inclusions. Our results demonstrate that the immunohistochemical profile of the recently described inclusions differs from that of Rosenthal fibers. Whether the novel inclusions are involved in congenital astrocyte dysfunction and cerebral malformation remains to be established.
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PMID:Immunohistochemical studies on the new type of astrocytic inclusions identified in a patient with brain malformation. 133 66

Cathepsin D expression was assessed by immunohistochemistry in 59 node-negative and 77 node-positive infiltrative ductal not otherwise specified (NOS) breast carcinomas and compared with overall survival at 90 months. Cancer cells in 60% (81/136) of the tumors expressed cathepsin D. In the stroma of 33% (18 of 55) cathepsin D negative tumors, numerous strongly cathepsin D positive, benign macrophage-like cells were found. Multivariate analysis showed no significant correlation of cathepsin D expression and overall survival for all patients for node-negative and node-positive patients and for patients with vimentin-positive and -negative tumors. However, in node-negative but not in node-positive patients, a trend for better survival for patients with cathepsin-positive vimentin-negative tumors and worse survival for those with cathepsin-positive vimentin-positive tumors was noted. Due to the low number of patients in these subgroups, neither trend reached significance. Cathepsin D expression was independent of patient age, size, and histologic grade of tumor, and vimentin expression. However, in the node-positive group, negative correlation of cathepsin D and vimentin expression was found. We suggest that prognostic significance of cathepsin D in infiltrative ductal NOS breast carcinomas may be associated with the pathway of its synthesis rather than with its mere presence in tumor cells.
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PMID:Cathepsin D in invasive ductal NOS breast carcinoma as defined by immunohistochemistry. No correlation with survival at 5 years. 133 83

Fibroblastoid synovial lining cells isolated from rheumatoid and other chronic inflammatory synovial tissue exhibit distinctive and sustained alterations in serial culture not commonly found in similarly cultured cells from osteoarthritic synovium. These are demonstrable using a multi-gene dot blot assay by labelling reverse transcribed fibroblast cDNA which is hybridized to plasmids containing relevant target gene inserts. Cultured synovial fibroblastoid cells from patients with chronic inflammatory synovitis expressed significantly higher levels of stromelysin, vimentin and TIMP-1 mRNA and lower levels of c-myc compared to cells isolated from osteoarthritis synovium although with considerable variation. Early fetal synovial lining cells were similar to cells from osteoarthritis synovium but vimentin expression was higher. Marked differences in patterns of gene expression between cell lines persisted through 10 serial passages over 6-8 months. In whole synovia, the average level of mRNA for stromelysin, vimentin, IL-4, IL-6, TIMP-1, cathepsin D, gelatinase, TGF alpha, c-fms and DR beta were preferentially expressed in inflammatory tissue while c-myc expression was higher in osteoarthritis synovium. Inflammatory synovium also expressed TNF alpha, IL-1 alpha, IL-1 beta, IL-2, c-sis, tissue plasminogen activator, CSF-1, and GM-CSF. This pattern resembles, in part, that found in cultured inflammatory fibroblasts but, in addition, gene products apparently reflecting the presence of activated monocytes and lymphocytes were detected. These results provide evidence that profiles of certain gene activation in cells from patients with inflammatory synovitis differ from those with non-inflammatory disease and suggest that the fibroblastoid cells are responsible for a considerable proportion of the altered phenotypic expression pattern in whole tissue. Furthermore, this modulated pattern of gene activation appears to be an intrinsic pro-inflammatory characteristic of the fibroblastoid cells initiated in response to chronic inflammation and persists for a prolonged period in the absence of other inflammatory cells.
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PMID:Sustained and distinctive patterns of gene activation in synovial fibroblasts and whole synovial tissue obtained from inflammatory synovitis. 809 Nov 28

Vimentin, p53 protein and cathepsin D positivity were assessed by immunohistochemistry, and oestrogen receptor (ER) by an enzyme immunoassay, in invasive lobular carcinomas (LC) of the breast. While vimentin was positive in only 5% (3/57) and p53 protein was positive only in 3% (2/63), cathepsin D was expressed in 86% (48/56) and ER in 78% (25/32). Classical LC were negative for p53 protein and all except one were cathepsin D positive. These results are in contrast to invasive ductal breast carcinomas (DC), where the reported average incidence of vimentin and p53 protein is much higher (19% and 33% respectively) and that of cathepsin D and ER lower (63% and 67% respectively). Thus lack of expression of vimentin and lack of p53 positivity together with high incidence of expression of cathepsin D and ER are more often associated with lobular than with ductal differentiation of invasive breast cancer. The results show that LC, distinguished morphologically, can further be defined by its immunohistochemical profile. This in turn may point to underlying biological differences between LC and DC.
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PMID:Immunohistochemical profile of invasive lobular carcinoma of the breast: predominantly vimentin and p53 protein negative, cathepsin D and oestrogen receptor positive. 829 Dec 22

Matrigel invasion assays were used to characterize the invasive abilities of five breast cancer cell lines. Reverse Transcription Polymerase Chain Reaction (RT-PCR) was used to detect the differential gene expression of estrogen receptor (ER), E-cadherin, vimentin and cathepsin D in these cell lines. Using mRNA differential display, we identified novel cDNA clones representing the partial sequences of genes overexpressed in the invasive MDA-MB-435 cells as compared to that of the less invasive MCF-7 cells. One of the cDNAs was homologous to reticulocalbin. The studies were repeated in all of the cell lines and the overexpression of this cDNA was confirmed by RT-PRC and Northern hybridization analysis. Reticulocalbin was expressed in the highly invasive breast cancer cell lines but was not expressed in poorly invasive ones. Although its function is still unknown, reticulocalbin is implicated in tumor cell invasiveness because of its differential expression in breast tumor cell lines.
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PMID:Differential display of reticulocalbin in the highly invasive cell line, MDA-MB-435, versus the poorly invasive cell line, MCF-7. 907 Feb 64

The wall structure of arterio-venous anastomoses in human glomus organs was studied by immunohistochemistry and immunoelectron microscopy. Smooth muscle cells of the epithelioid type I and of the dense type II could be found in the media. The immunohistochemical study confirmed the immunopositivity of both smooth muscle cell types for alpha-smooth muscle actin, vimentin, and smooth muscle myosin. All smooth muscle cells also stained positively for caveolin, a recently described structural protein of microvesicles present in selected epithelial and nonepithelial cells. The immunoreactivity for cathepsin D, however, was much higher in the type I cells than in the type II cells. Immunoelectron microscopy revealed that type I cells contain loose arrays of alpha smooth muscle actin positive microfilaments, sometimes arranged in small bundles, whereas the dense medial smooth muscle cells of the type II have tightly packed actin filaments. Only type I cells contained cathepsin D positive lysosomes. The data suggest that two types of phenotypic variants of vascular smooth muscle cells in the human arterio-venous anastomosis exist: a more "synthetic" type I cell and a more contractile type II cell.
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PMID:Immunoelectron microscopical characterization of the epithelioid type of smooth muscle cells in human glomus organs. 927 72

Pituitary carcinomas are only defined by their metastatic growth, which may be intracranial or systemic. To establish further morphological and immunohistochemical differences between pituitary carcinomas and adenomas, 19 ACTH-secreting adenomas (10 non invasive and 9 invasive) and 2 ACTH-secreting carcinomas with their metastases were studied for expression of the intermediate filaments keratin and vimentin and the tumor-associated antigens Ki67, proliferating cell nuclear antigen (PCNA), epidermal growth factor (EGF), cathepsin D, p53, and carcinoembryonic antigen (CEA). Immunohistochemistry was performed using avidin-biotin techniques on formalin-fixed, paraffin-embedded tissue. With the exception of one noninvasive pituitary adenoma, one carcinoma, and the metastases, all tumors contained keratin; none contained vimentin. All tumors stained negative for CEA and p53. Eleven (58.5%) adenomas and both pituitary carcinomas contained Ki67-positive nuclei; 14 (74%) adenomas and one carcinoma revealed PCNA. No correlation was found between the two markers. Seven (38%) adenomas showed a labeling index <1 % for cathepsin D, whereas none of the carcinomas or metastases did so. EGF was found in 7 (38%) adenomas and in both carcinomas. A tendency to a higher rate of EGF positivity in the invasive adenomas was observed. The metastases showed a higher labeling index, and far more intense staining results for Ki67, PCNA, and EGF than the primary tumor. The metastases also had a higher proliferation rate and growth factor content than the carcinoma itself.
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PMID:Proliferation Markers and EGF in ACTH-Secreting Adenomas and Carcinomas of the Pituitary. 1211 89

Hypoxia-inducible factor 1 (HIF-1) transactivates genes the products of which mediate tumor angiogenesis and glycolytic metabolism. Overexpression of the HIF-1 alpha subunit, resulting from intratumoral hypoxia and genetic alterations, has been demonstrated in common human cancers and is correlated with tumor angiogenesis and patient mortality. Here we demonstrate that hypoxia or HIF-1 alpha overexpression stimulates Matrigel invasion by HCT116 human colon carcinoma cells, whereas this process is inhibited by a small interfering RNA directed against HIF-1 alpha. We show that HIF-1 regulates the expression of genes encoding cathepsin D; matrix metalloproteinase 2; urokinase plasminogen activator receptor (uPAR); fibronectin 1; keratins 14, 18, and 19; vimentin; transforming growth factor alpha; and autocrine motility factor, which are proteins that play established roles in the pathophysiology of invasion. Neutralizing antibodies against uPAR block tumor cell invasion induced by hypoxia or HIF-1 alpha overexpression. These results provide a molecular basis for promotion of the invasive cancer phenotype by hypoxia and/or HIF-1 alpha overexpression.
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PMID:Regulation of colon carcinoma cell invasion by hypoxia-inducible factor 1. 1261 33

The major neuropathological features of the transmissible spongiform encephalopathies (TSEs) are well documented, however, the underlying molecular events are poorly defined. We have applied cDNA expression arrays and quantitative RT-PCR to the study of gene expression in the brain, and more specifically in the hippocampus, of the well-characterized ME7/CV mouse model of scrapie. The number of genes showing consistent, scrapie-associated changes in expression was limited, and was primarily restricted to glial-associated genes. Increased expression of genes encoding glial fibrillary acidic protein, vimentin, complement component 1q (alpha and beta polypeptides), cathepsin D, clusterin and cystatin C was evident in the hippocampus from 170 days after inoculation (dpi), with expression increasing thereafter to terminal disease (225-235 dpi). Elevation of gene expression preceded clinical disease by approximately 30 days, and coincided with a 20-day period in the ME7/CV model during which 50% of the CA1 hippocampal neurones are lost. Increased expression of cystatin C, an inhibitor of lysosomal cysteine proteases, is a novel finding in the context of TSE neuropathology and was confirmed by Western analysis and immunocytochemistry.
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PMID:Identification of up-regulated genes by array analysis in scrapie-infected mouse brains. 1548 32

Sarcoplasmic masses contain disorganized myofibrillar material and are a striking feature of myotonic dystrophy. However their significance is still unclear. Using immunocytochemistry we studied the expression of cytoskeletal proteins (desmin and vimentin), dystrophin, markers of myogenic differentiation (foetal myosin, neural cell adhesion molecule, bcl-2, insulin-like growth factor-I, fibroblast growth factor, retinoblastoma protein and myoD1), cell cycle regulators (Cdk2, p16, p27 and p57) and muscle proteases (ubiquitin, micro and m calpain and cathepsin D) in muscle biopsies from four patients with myotonic dystrophy. Sarcoplasmic masses were strongly positive for desmin, neural cell adhesion molecule, bcl-2, insulin-like growth factor I, retinoblastoma protein and p57, weakly positive for dystrophin and p16 and negative for vimentin, fibroblast growth factor, myoD1, Cdk2 and p27. Immunoreactivity for foetal myosin was detected only in a few fibres (< 1%). Our data suggest that the late myogenic differentiation programme is activated in sarcoplasmic masses although these areas do not reach complete maturation.
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PMID:Expression of late myogenic differentiation markers in sarcoplasmic masses of patients with myotonic dystrophy. 1563 30


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