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

---

Query: EC:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three T cell clones derived from rabies virus-immunized BALB/c mice were analysed for specificity and function. The clones proved to be broadly cross-reactive by responding to different rabies virus isolates (PM, ERA, CVS, HEP) and other representatives of the genus Lyssavirus, like the Duvenhage-6 (DUV6) and Mokola (MOK) viruses. The clones detected three different epitopes: an epitope expressed on the matrix protein (M) shared by PM, HEP, MOK and DUV6 viruses (clone AA8), an epitope expressed on the M-protein shared by PM, ERA, CVS, HEP and MOK viruses (clone 35A) and finally an epitope expressed on the glycoprotein (G-protein) shared by PM, ERA, CVS, HEP and MOK viruses (clone BG2). Antigen recognition of all clones proved to be MHC-restricted and they all displayed the CD4+ CD8- phenotype. Intravenous inoculation of the T cells in syngeneic mice, which had been injected intracutaneously in the ear with HEP virus, resulted in a localized DTH reaction characteristic for TH1 cells. In vitro, the clones were able to provide help to rabies virus-primed B cells, resulting in the production of virus-specific antibodies directed against all the four structural proteins of rabies virus. Further analysis of this antibody response revealed that part of it was directed against antigenic determinants of the G-protein which induce virus neutralizing antibody.
...
PMID:Rabies virus cross-reactive murine T cell clones: analysis of helper and delayed-type hypersensitivity function. 196 28

Synthesis of measles virus proteins in primary and chronic infection of L-41 and HEP-2 cells was studied by radioimmunoprecipitation test and polyacrylamide gel electrophoresis. Synthesis of measles virus main structural proteins, H, P, NP, and M, was found to occur in chronically infected cells. Persistence of measles virus in the systems under study was shown not to be accompanied by changes in electrophoretic mobility of virus polypeptides as compared with proteins synthesized in primary infection. NP protein of the original virus, however, differed significantly from NP protein of the persisting virus in its charge which indicated aminoacid replacements apparently due to mutations of the appropriate region of the virus genome. The mechanism of measles virus persistence in these systems was shown not to be associated with disorders in matrix protein synthesis. Use of monoclonal antibodies in fluorescent antibody technique and radioimmunoprecipitation revealed the stability of a number of antigenic determinants in persisting measles virus in L-41 and HEP-2 cell cultures.
...
PMID:[Synthesis of measles virus proteins in chronically infected human cell cultures]. 376 67

We investigated unusual structures produced in BHK-21 cells infected with rabies virus (HEP-Flury strain). Sellers' staining of the cells revealed, in addition to Negri body-like structures (inclusion bodies), production of a fuchsin-stained cytoplasmic structure (FCPS) which encircled the nucleus. The frequency of the FCPS-forming cells increased as replication progressed. The FCPS was different from the inclusion body because the former contained the viral glycoprotein (G) and matrix protein (M2) antigens, while the latter contained nucleocapsid antigens. In the early phase of infection, we observed accumulation of viral envelope antigens in a cytoplasmic structure that was considered to be expanded rough endoplasmic reticulum (rER) because of its concomitant increase in BiP content. Time-course studies suggested that the envelope antigen-containing structure, which was not stained with basic fuchsin, translocated to the perinuclear region to form the FCPS. FCPS formation was dependent on incubation temperature and was decreased at 30 degrees C, while the development of virus-induced cytopathic effect (CPE) was delayed. When the incubation temperature was shifted up to 37 degrees C, FCPS formation was induced again and progression of CPE was accelerated in approximate proportion to the increasing number of FCPS-positive cells. From these studies, we conclude that viral G proteins gradually accumulate in the rER with M2 protein and the expanded rER converts eventually into the FCPS, which may be closely related to accelerated host cell death.
...
PMID:Studies on unusual cytoplasmic structures which contain rabies virus envelope proteins. 881 Oct 13

We have used exon amplification to identify putative transcribed sequences from an 823-kb contig consisting of 28 cosmids that form a minimum tiling path from the interval 19p12-p13.1. This region contains the genes responsible for multiple epiphyseal dysplasia (MED) and pseudoachondroplasia (PSACH). We have trapped 66 exons (an average of 2.4 exons per cosmid) from pools of 2 or 3 cosmids. The majority of exons (51.5%) show only weak similarity or no similarity (36.3%) to sequences in current databases. Six of 8 exons examined from these groups, however, show cross-species sequence conservation, indicating that many of them probably represent authentic exons. Eight exons show identity or significant similarity to ESTs or known genes, including the human TNF receptor 3 '-flanking region gene, human epoxide hydrolase (EPHX), human growth/differentiation factor (GOF-1), human myocyte-specific enhancer factor 2, the rat neurocan gene, and the human cartilage oligomeric matrix protein gene (COMP). Mutations in this latter gene have recently been shown to be responsible for MED and PSACH.
...
PMID:The identification of exons from the MED/PSACH region of human chromosome 19. 883 48

The protein composition of the nuclear matrix is both tissue and cell type specific, and it undergoes changes with differentiation and transformation. In the present study, nuclear matrix proteins of EGFR-antisense transfected glioblastoma cell lines, U87 and U343, were compared with untransfected cell lines using two dimensional-gel electrophoresis. After EGFR-antisense transfection, the protein compositions of the nuclear matrices in both cell lines were different. Several nuclear proteins were only found in EGFR-antisense transfected cell lines. There was no difference in NuMA expression in the transfected and untransfected cell lines. These results suggest that EGFR-antisense reduced tumorigenicity on human glioblastoma cells by changing nuclear matrix protein compositions.
...
PMID:Comparison of nuclear matrix proteins between EGFR-antisense transfected and untransfected glioblastoma cells. 985 91

Previous work shows that osteopontin has a role during matrix reorganization after tissue injury including vascular conditions such as atherosclerosis and restenosis following angioplasty. In vitro, osteopontin promotes activities such as adhesion and migration but the mechanisms that regulate the expression of this matrix protein remain essentially unknown. This study examined if the ERK signaling pathway is involved in injury-induced osteopontin expression in cultured rat aortic smooth muscle cells. Northern and Western blotting demonstrated a marked activation of osteopontin expression in response to injury. Treating the cells with PD98059, a specific MEK1 inhibitor, prior to injury, blocked this upregulation. MEK1 phosphorylates ERK1/ERK2, which belong to the family of mitogen-activated protein kinases. We conclude that ERK1/ERK2 are involved in the regulation of osteopontin expression in cultured vascular smooth muscle cells.
...
PMID:Injury-induced osteopontin gene expression in rat arterial smooth muscle cells is dependent on mitogen-activated protein kinases ERK1/ERK2. 1171 72

Evidence suggests that the arachidonic acid metabolite of 12-lipoxygenase, 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE), not only mediates the effects of angiotensin II (AngII), but also has direct effects on hypertrophy and matrix protein production in vascular smooth muscle cells (VSMCs). This study is aimed at identifying the signaling pathways involved in these events. Treatment of porcine VSMCs with 12(S)-HETE led to the activation of Ras and p38 MAPK. It also stimulated phosphorylation, DNA-binding activity, and transactivation of the transcription factor cAMP response element (CRE)-binding protein. In addition, 12(S)-HETE induced transcription from a fibronectin promoter containing multiple CREs. AngII also induced transactivation of CRE-binding protein and transcription from the fibronectin promoter. A specific p38 MAPK inhibitor (SB202190) as well as a dominant-negative Ras mutant (Ras-N17) blocked both 12(S)-HETE and AngII effects. In addition, inhibitors of lipoxygenase also blocked AngII effects. Both 12(S)-HETE and AngII increased cellular hypertrophy with similar potency, and this was significantly blocked by SB202190. Stable overexpression of murine leukocyte-type 12/15-lipoxygenase in VSMCs increased the levels of cell-associated 12(S)-HETE as well as basal activity of both ERK and p38 MAPKs. Furthermore, these 12-lipoxygenase-overexpressing cells displayed significantly greater cellular hypertrophy relative to mock-transfected cells. These results show for the first time that oxidized lipids such as 12(S)-HETE can induce VSMC growth and matrix gene expression and mediate growth factor effects via activation of the Ras-MAPK pathway and key target transcription factors.
...
PMID:The oxidized lipid and lipoxygenase product 12(S)-hydroxyeicosatetraenoic acid induces hypertrophy and fibronectin transcription in vascular smooth muscle cells via p38 MAPK and cAMP response element-binding protein activation. Mediation of angiotensin II effects. 1178 49

Transforming growth factor beta (TGF-beta) activates Ras/MAPK signaling in many cell types. Because TGF-beta and BMP-2 exert similar effects, we examined if this signaling is stimulated by both factors and analyzed the relationship between this signaling and the Smads in osteoblasts. BMP-2 and TGF-beta stimulated Ras, MAPK, and AP-1 activities. The DNA binding activities of c-Fos, FosB/Delta FosB, Fra-1, Fra-2, and JunB were up-regulated whereas JunD activity was decreased. c-Fos, FosB/Delta FosB, and JunB were associated with Smad4. The stimulation of AP-1 by BMP-2 and TGF-beta was dependent on Smad signaling, and anti-Smad4 antibody interfered with AP-1 activity. Thus, BMP-2 and TGF-beta activate both Ras/MAPK/AP-1 and Smad signaling in osteoblasts with Smads modulating AP-1 activity. To determine the roles of MAPK in BMP-2 and TGF-beta function, we analyzed the effect of ERK and p38 inhibitors on the regulation of bone matrix protein expression and JunB and JunD levels by these two factors. ERK and p38 mediated TGF-beta suppression of osteocalcin and JunD as well as stimulation of JunB. p38 was essential in BMP-2 up-regulation of type I collagen, fibronectin, osteopontin, osteocalcin, and alkaline phosphatase activity whereas ERK mediated BMP-2 stimulation of fibronectin and osteopontin. Thus, ERK and p38 differentially mediate TGF-beta and BMP-2 function in osteoblasts.
...
PMID:Signal transductions induced by bone morphogenetic protein-2 and transforming growth factor-beta in normal human osteoblastic cells. 1185 97

During influenza virus infection, viral ribonucleoproteins (vRNPs) are replicated in the nucleus and must be exported to the cytoplasm before assembling into mature viral particles. Nuclear export is mediated by the cellular protein Crm1 and putatively by the viral protein NEP/NS2. Proteolytic cleavage of NEP defines an N-terminal domain which mediates RanGTP-dependent binding to Crm1 and a C-terminal domain which binds to the viral matrix protein M1. The 2.6 A crystal structure of the C-terminal domain reveals an amphipathic helical hairpin which dimerizes as a four-helix bundle. The NEP-M1 interaction involves two critical epitopes: an exposed tryptophan (Trp78) surrounded by a cluster of glutamate residues on NEP, and the basic nuclear localization signal (NLS) of M1. Implications for vRNP export are discussed.
...
PMID:Crystal structure of the M1 protein-binding domain of the influenza A virus nuclear export protein (NEP/NS2). 1297 Jan 77

We examined the effect of magnetic force on differentiation of cultured human osteoblasts. Magnetic microparticles (MPs) were introduced into the cytoplasm of a human osteoblast cell line and the cells were cultured in a magnetic field (MF) in group MP-MF. Three groups of controls were used: cells without MPs were cultured out of MF (group C), cells without MPs were cultured in MF (group MF), and cells with MPs were cultured out of MF (group MP). The cells in group MP-MF became larger and were elongated along the axis of the magnetic poles. Appearance of alkaline phosphatase (AlPase) activity, formation of bone nodules, and calcium deposition were accelerated depending on the intensity of the magnetic field. It takes longer culture in the other three groups to exhibit these changes. Core-binding factor A1 (Cbfa1: transcription factor for osteoblast differentiation) and osteocalcin (a bone-matrix protein involved in controlling osteogenesis) were expressed earlier or stronger in group MP-MF than the other groups. Then we compared phosphorylation of mitogen-activated protein kinase (MAPK) between group MP-MF and group C. Phosphorylation of p38(MAPK) (p38) was increased in group MP-MF, while total p38 as well as total and phosphorylated forms of MAPK/ERK 1/2 and SAPK/JNK were not changed between the two groups. When a p38 inhibitor, SB 203580, was added to the culture medium in group C, AlPase activity, formation of bone nodules, and calcium deposits were completely inhibited. On the other hand, they were inhibited only partially by a MAPK/ERK 1/2 inhibitor, U-0126. Based on these results, it is concluded that (1) osteoblast differentiation is accelerated by a magnetic force, (2) this acceleration is mainly attributed to the activation of p38 phosphorylation, and (3) the stimulus induced by a magnetic field offers a new approach to osteoblast differentiation.
...
PMID:Physical stress by magnetic force accelerates differentiation of human osteoblasts. 1457 91


1 2 3 4 5 6 Next >>

---