Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Major histocompatibility complex (MHC) class I molecules are integral membrane proteins present on virtually all vertebrate cells and consist of a heterodimer between the highly polymorphic alpha-chain and the beta 2-microglobulin (beta 2-m) protein of relative molecular mass 12,000 (ref. 1). These cell-surface molecules play a pivotal part in the recognition of antigens, the cytotoxic response of T cells, and the induction of self tolerance. It is possible, however, that the function of MHC class I molecules is not restricted to the immune system, but extends to a wide variety of biological reactions including cell-cell interactions. For example, MHC class I molecules seem to be associated with various cell-surface proteins, including the receptors for insulin, epidermal growth factor, luteinizing hormone and the beta-adrenergic receptor. In mice, class I molecules are secreted in the urine and act as highly specific olfactory cues which influence mating preference. The beta 2-m protein has also been identified as the smaller component of the Fc receptor in neonatal intestinal cells, and it has been suggested that the protein induces collagenase in fibroblasts. Cells lacking beta 2-m are deficient in the expression of MHC class I molecules, indicating that the association with beta 2-m is crucial for the transport of MHC class I molecules to the cell surface. The most direct means of unravelling the many biological functions of beta 2-m is to create a mutant mouse with a defective beta 2-m gene. We have now used the technique of homologous recombination to disrupt the beta 2-m gene. We report here that introduction of a targeting vector into embryonic stem cells resulted in beta 2-m gene disruption with high frequency. Chimaeric mice derived from blastocysts injected with mutant embryonic stem cell clones transmit the mutant allele to their offspring.
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PMID:Germ-line transmission of a disrupted beta 2-microglobulin gene produced by homologous recombination in embryonic stem cells. 268 7

The clinical course of sarcoidosis is varying and unpredictable. Once the diagnosis has been made, the clinician needs simple tests to detect and predict remission or progression, to determine whether treatment is effective or not, and to assess the clinical activity of the disease. Sarcoidosis is a multisystem disease, but the lungs are almost always involved. Traditionally, the clinical management has therefore included chest X-rays and lung function studies. Extrapulmonary lesions have been followed in different ways. Sensitive and reproducible biochemical tests would be helpful in evaluating the clinical course of patients with sarcoidosis, if they measure functions related to the granulomatous inflammation. This review will deal with measurements of serum and urinary calcium, and 1,25-dihydroxyvitamin D. The usefulness of single and serial determinations of lysozyme, angiotensin converting enzyme, beta 2-microglobulin, collagenase, carboxypeptidase and glucuronidase in serum, bronchoalveolar lavage fluid, and other biological fluids will be discussed.
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PMID:Biochemical markers in sarcoidosis. 302 7

Immunolocalization of matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) in periarticular tissues of beta 2-microglobulin amyloidosis patients was investigated. MMP-1 (interstitial collagenase) the most strongly expressed of the MMPs, was localized in the synovial lining cells, mesenchymal cells in granulation tissue and nodular amyloid deposits, and chondrocytes within areas of cartilage erosion. Expression of MMP-1 was correlated with the degree of macrophage infiltration and synovial cell hyperplasia, but it was not correlated with the degree of amyloid deposition or haemodialysis period. Expression of MMP-1 appeared more intense than that of TIMP-1 and TIMP-2 in highly inflammatory cases. MMP-2 was mildly expressed in the interstitial fibroblasts and MMP-3 was faintly stained in the extracellular matrix of the synovial membrane. MMP-9 (gelatinase B) was found to be strongly positive in the osteoclasts which increased in the progressing osteolytic lesion from the destructive arthropathy. These results suggest involvement of MMPs in inflammation with an imbalance between expression of MMPs and TIMPs being closely related to pathogenesis of the destructive arthropathy.
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PMID:Increased matrix metalloproteinases as possible cause of osseoarticular tissue destruction in long-term haemodialysis and beta 2-microglobulin amyloidosis. 864 67

We evaluated the role of tissue inhibitors of metalloproteinase-1 (TIMP-1) in patients with diabetic nephropathy by comparing the serum and urine TIMP-1 levels with those of renal biopsy specimens. A total of 35 diabetic patients were divided into four groups, D0, DI, DII and DIII-IV, according to the severity of diffuse glomerular lesions using Gellman's criteria. Using serum and 24-hour urine specimens, TIMP-1 was measured by a sandwich enzyme immunoassay. Serum and urinary TIMP-1 showed significant increases in association with the progress of glomerular diffuse lesions. There was no correlation between serum TIMP-1 and serum creatinine, creatinine clearance, serum and urinary beta 2-microglobulin, urinary NAG, HbA1c, or urinary TIMP-1. There was a significant correlation between urinary TIMP-1 and urinary albumin, and was a significant correlation between urinary TIMP-1 and urinary NAG. We conclude that TIMP-1 has a potential role in the regulation of glomerular matrix accumulation in diabetic nephropathy.
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PMID:Role of tissue inhibitors of metalloproteinase in diabetic nephropathy. 872 33

In order to study decidual proteins produced during pregnancy, decidual cells were isolated from term placental membranes by collagenase digestion and Percoll gradient centrifugation. Serum-free CMRL-1066 medium, conditioned for 148 h with the purified decidual cells, was collected and concentrated by ultrafiltration and applied to a Sephadex G-50 column. The protein-containing fractions from the column were concentrated, dialyzed, lyophilized, applied to sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and transferred to a polyvinylidene difluoride membrane, followed by sequencing. Superoxide dismutase and two new members of the decidual protein family, beta 2-microglobulin precursor and ubiquitin, were identified by 100% N-terminal sequence homology, and similarities of molecular weights and residue contents.
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PMID:Production of superoxide dismutase, beta 2-microglobulin and ubiquitin by human term decidua in vitro. 936 43

To elucidate the mechanism of neutrophil dysfunction in patients with maintenance hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD), intracellular enzyme activity such as oxidative burst, elastase, cathepsin, and collagenase, was investigated. Response of enzyme activity to in vitro addition of TNF-alpha, which is known to have a powerful priming effect on neutrophils, was also evaluated. Peripheral blood from 15 HD and 15 CAPD patients was washed and incubated with Cell Probe, an indicator for intracellular enzyme activity. Mean fluorescent intensity of neutrophils, which represents neutrophil enzyme activity, was measured by flowcytometry. In HD group, unstimulated enzyme activity was similar to that of control, but activity after addition of TNF-alpha was significantly lower than the control. In the group of CAPD, enzyme activity without stimulation was not different from that of control, and in TNF-alpha stimulated neutrophils, only elastase activity was lower than control. Many of the enzyme activities after stimulation were lower in HD than in CAPD. Response to in vitro addition of TNF-alpha was diminished in both dialysis groups, but more prominent in HD neutrophils. Duration of dialysis, serum concentration of beta 2-microglobulin (beta 2-MG) and parathyroid hormone (PTH) was significantly related inversely to intracellular enzyme activity in HD patients. To the contrary, in CAPD group, although beta 2-MG and PTH showed similar negative correlation, duration of dialysis was not related to enzyme activity. These results indicate that neutrophils in patients with maintenance dialysis have diminished intracellular oxidative burst, elastase, and cathepsin activity. Especially, impaired response to TNF-alpha closely related to neutrophil dysfunction in dialysis patients.
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PMID:[Flowcytomeric analysis on neutrophil intracellular enzyme activity in patients on hemodialysis and continuous ambulatory peritoneal dialysis]. 1069 98