Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The UHF fraction from NIL 8 hamster embryo fibroblasts contains the LETS protein and several other major proteins. It exhibits three enzymatic activities in significant amounts: 5'-nucleotidase, alkaline phosphatase, and galactosyl transferase. The latter two appear to be different from the membrane-bound enzymes. This fraction is heavily stained with ruthenium red, a dye specific for the cell coat in intact cells. A comparable fraction from hamster sarcoma virus-transformed cells exhibits a similar overall protein composition but lacks at least three major proteins, including the LETS protein. Compared to NIL 8 cells, the distribution of alkaline phosphatase in fractions from these cells is different, and the level of galactosyl transferase in the UHF is much reduced.
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PMID:Cell surface coat of hamster fibroblasts. 29 62

An earlier study by our group demonstrated significant amelioration of hypotension, hypoglycemia, and acidosis in dogs treated with purified human plasma fibronectin prior to induction of endotoxic shock. The present study was completed to determine whether treatment with purified human plasma fibronectin 1 hr after induction of endotoxic shock would provide similar benefits. To this end, selected hemodynamic, pulmonary, acid-base, metabolic, hematological, and serum chemistry parameters were monitored for 6 hours in two groups of anesthetized dogs in Escherichia coli endotoxic shock. One group was given an intravenous injection of purified human plasma fibronectin, and the other received an equal volume of saline 1 hr after shock induction. Between-group analysis of the data revealed no significant differences between any parameter excepting modest differences in plasma glucose, albumin, alkaline phosphatase, and BUN concentrations. However, even these differences, although statistically significant, were sporadic and unimpressive. This study suggested that treatment of dogs with fibronectin during gram-negative endotoxic shock was not efficacious.
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PMID:Effect of fibronectin supplementation in endotoxic shock in the dog. 365 96

A male-specific genetic linkage map of nine loci on bovine Chromosome (Chr) 2 (BTA2) was constructed from 306 offspring belonging to six paternal half-sib families. Loci studied were the structural genes for liver/bone/kidney alkaline phosphatase (ALPL). Gardner-Rasheed feline sarcoma (v-fgr) oncogene homolog (FGR), alpha-L-fucosidase 1 (FUCA1), and fibronectin 1 (FN1), and the microsatellite loci ARO28, DU17S2, DU17S3, DU17S4, and DU17S5. Genotyping was performed by restriction fragment length polymorphism (RFLP) for structural genes and polymerase chain reaction (PCR) for the microsatellites. Two genetically independent linkage groups were identified. The order of genes in the first linkage group, L31, is (ARO28-FN1)-FGR-FUCA1-ALPL, covering a map distance of 34.1 cM between terminal markers. The second linkage group, L32, consists of DU17S2-DU17S5-DU17S4-DU17S3 and is 41.3 cM in length. Genetic linkage between FN1 and FGR confirms previous physical assignment of these genes to the same synteny group. Currently, the genetic linkage of FN1 and FGR is unique to cattle and thus localizes a site of chromosomal evolution to a 22-cM interval between the two loci.
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PMID:A genetic map of nine loci on bovine chromosome 2. 800 Jan 37

Multilocus linkage analysis has suggested that the Waardenburg syndrome type 1 (WS1) locus is flanked by placental alkaline phosphatase (ALPP) and fibronectin 1 (FN1). We used fluorescence in situ hybridization (FISH) to map ALPI (intestinal alkaline phosphatase) to 2q36.3-q37.1 and FN1 to 2q34. FISH also showed that a WS1 patient with a de novo interstitial deletion of 2q35-q36.1 retained both API and FN1 on the deleted chromosome. The human PAX3 gene has been shown previously to be mutated in at least two WS1 patients. We mapped a PCR product from the PAX3 gene to 2q35 and found it was absent in the deleted chromosome. Thus, our FISH mapping results confirm the conclusions from previous linkage analysis and support the conclusion that mutation of the PAX3 gene can cause Waardenburg syndrome.
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PMID:In situ hybridization applied to Waardenburg syndrome. 844 34

Recently, calcium sulfate dihydrate has been demonstrated as safe biodegradable osteoconductive bone void filler. However, its exact mechanism of action on bone cells is yet unknown. In this study, the influence of gypsum on gene expression and proliferation of MC3T3-E1 mouse pre-osteoblastic cells was investigated. Cells were cultured on gypsum disc, slice, polymethylmethacrylate (PMMA), or plastic culture plate for 15 days. Cell viability, alkaline phosphatase (ALP) activity and expression profile of 15 genes involved in bone metabolism were measured in cultures. Cell proliferation on gypsum was increased by almost 2-fold, while an inhibitory effect of PMMA on proliferation rate of osteoblasts was noted. Cells cultured on gypsum disc surface exhibited an increased ALP activity and markedly different gene expression profile. Quantitative real-time PCR data indicated the expression of genes that might provide a basis for an osteoinductive potential. MC3T3-E1 cells expressed genes typical of bone fracture healing like type II collagen and fibronectin 1. These effects might be related to the calcium content of gypsum and mediated likely via SMAD3. Our results suggest that gypsum can support new bone formation by its calcium content and modulatory effect on gene expression profile of bone cells.
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PMID:Effect of gypsum on proliferation and differentiation of MC3T3-E1 mouse osteoblastic cells. 1699 72

The periodontal ligament is a multifunctional soft connective tissue, which functions not only as a cushion supporting the teeth against occlusal force, but is also a source of osteogenic cells that can regenerate neighboring hard tissues. Periodontal ligament cells (PDL cells) contain heterogeneous cell populations, including osteogenic cell progenitors. However, the precise mechanism underlying the differentiation process remains elusive. Cell differentiation is regulated by the local biochemical and mechanical microenvironment that can modulate gene expression and cell morphology by altering actin cytoskeletal organization mediated by Rho-associated, coiled-coil containing protein kinase (ROCK). To determine its role in PDL cell differentiation, we examined the effects of ROCK on cytoskeletal changes and kinetics of gene expression during osteogenic differentiation. PDL cells were isolated from human periodontal ligament on extracted teeth and cultured in osteogenic medium for 14 days. Y-27632 was used for ROCK inhibition assay. Osteogenic phenotype was determined by monitoring alkaline phosphatase (ALP) activity and calcium deposition by Alizarin Red staining. ROCK-induced cytoskeletal changes were examined by immunofluorescence analysis of F-actin and myosin light chain 2 (MLC2) expression. Real-time PCR was performed to examine the kinetics of osteogenic gene expression. F-actin and phospho-MLC2 were markedly induced during osteogenic differentiation, which coincided with upregulation of ALP activity and mineralization. Subsequent inhibition assay indicated that Y-27632 significantly inhibited F-actin and phospho-MLC2 expression in a dose-dependent manner with concomitant partial reversal of the PDL cell osteogenic phenotype. PCR array analysis of osteogenic gene expression indicated that extracellular matrix genes, such as fibronectin 1, collagen type I and III, and biglycan, were significantly downregulated by Y27632. These findings indicated crucial effects of ROCK in cytoskeletal reorganization and differentiation of PDL cells toward osteogenic cells. ROCK contributes to induction of osteogenic differentiation by synergistic increases in extracellular matrix gene expression in PDL cells.
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PMID:Osteogenic differentiation regulated by Rho-kinase in periodontal ligament cells. 2527 79

Bronchopulmonary dysplasia (BPD) is a syndrome of respiratory distress caused by chronic lung injury, primarily in preterm infants. miR-206 and fibronectin 1 (FN1) are associated with the development of BPD. The present study used rat type II alveolar epithelial cells (AECII) to investigate the underlying mechanisms of BPD. AECII were isolated using a primary cell culture prior to alkaline phosphatase staining and immunofluorescence of surfactant protein C (SP-C). These were used to verify the presence of AECII. AECII were then divided into four groups, which were transfected with four different plasmids. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine the relative expression of miR-206 in the each group. The gene and protein expression level of FN1 was detected by RT-qPCR and immunofluorescence. The proliferation of AECII in each of the four groups was evaluated using an MTT assay 48 h following transfection. The percentage of apoptotic cells was determined by flow cytometric analysis. The present study demonstrated that upregulation of miR-206 decreased the expression of FN1 (P<0.05) and low levels of miR-206 led to increased expression of FN1 (P<0.05) in AECII. Furthermore, the forced expression of miR-206 suppressed proliferation and promoted apoptosis of AECII while downregulation of miR-206 had the opposite effect (P<0.05). The results of the current study provide valuable insights into the prevention of BPD and suggest that miR-206 may be used as a potential molecular target for BPD therapy in the future.
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PMID:miR-206 inhibits FN1 expression and proliferation and promotes apoptosis of rat type II alveolar epithelial cells. 2858 94