Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this report is to demonstrate the expression of very recently identified surface antigens on CD34+ and AC133+ bone marrow (BM) cells. Coexpression analysis of AC133 and defined antigens on CD34+ BM cells revealed that the majority of the CD164+, CD135+, CD117+, CD38low, CD33+, and CD71low cells resides in the AC133+ population. In contrast, most of the CD10+ and CD19+ B cell progenitors and a fraction of the CD71high population are AC133-, indicating that CD34+AC133+ cells are enriched in primitive and myeloid progenitor cells, whereas CD34+AC133- cells mainly consist of B cell and late erythroid progenitors. This corresponds to the highly reduced percentage of CD10+ B cells and the absence of CD71high erythroid progenitors on AC133+ selected BM cells. A portion of 0.2-0.7% of the AC133+ selected cells do not coexpress CD34. These cells are very small and define a uniform CD71-, CD117-, CD10-, CD38low, CD135+, HLA-DRhigh, CD45+ population with unknown delineation. Four color analysis on CD34+CD38- BM cells revealed that virtually all of these primitive cells express AC133. Using an improved liposome-enhanced labeling technique for the staining of weakly expressed antigens, subsets of this population could be identified which express the angiopoietin receptors TIE (67.6%) and TEK (36.8%), the vascular endothelial growth factor receptors FLT1 (7%), FLT4 (3.2%), and KDR (10.4%), or the receptor tyrosine kinases HER-2 (15.4%) and FLT3 (CD135; 77.6%). Our results suggest that the CD34+CD38- population is heterogeneous with respect to the expression of the analyzed receptor tyrosine kinases.
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PMID:Expression of novel surface antigens on early hematopoietic cells. 1037 8

TEK (TIE2) and TIE (TIE1) are structurally related receptor tyrosine kinases expressed in endothelial cells and their precursors. Genetic studies in the mouse have revealed essential functions of both receptors in angiogenic expansion of the vasculature during development. As previously shown, mouse embryos homozygous for a disrupted Tek allele die by day 10.5 of embryogenesis due to endocardial defects, hemorrhaging, and impaired vascular network formation. Furthermore, TIE is required cell autonomously for endothelial cell survival and extension of the vascular network during late embryogenesis. Here we have investigated possible redundancy in the TEK and TIE signalling pathways during vascular development. Vasculogenesis proceeds normally in embryos lacking both TEK and TIE, although such embryos die early in gestation of multiple cardiovascular defects. Mosaic analysis revealed an absolute requirement for TEK in the endocardium at E10.5, whereas TEK and TIE are dispensable for the initial assembly of the rest of the vasculature. In contrast, both receptors are required in the microvasculature during late organogenesis and in essentially all blood vessels of the adult. This analysis demonstrates essential functions for TEK and TIE in maintaining the integrity of the mature vasculature.
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PMID:Interaction of the TEK and TIE receptor tyrosine kinases during cardiovascular development. 1049 91

In this study of two common housing systems of dairy cattle, the tie-in system and the loose housing system, check lists were created to evaluate whether these husbandry systems fulfill the needs of the animals. Furthermore, a combination of questionnaires and interviews were employed to assess the qualification of dairy stockmen to handle the animals. These checklists should provide a useful tool for those persons involved in the examination of husbandry systems, both by providing a written record and by providing a clear outline of all the points that need to be covered during such an examination. The study, done in the way of an explorative analysis of data, included 22 farms (14 with tie-in systems and 8 with loose housing systems) and a total of 802 animals. With regard to the economic effects of poor management and housing conditions, several interesting and statistically noteworthy correlations emerged. TIE-IN SYSTEM: Positive correlations were found between severity of behavioural abnormalities (behave)and number of injuries due to husbandry system (injury); injury and number of inseminations per pregnancy (preg); injury and age of cow (age); preg and cell count of milk (cell). Negative correlations were found between cell and milk yield (milk) as well as between the qualification of stockmen (equal) and inappropriate technical design of the housing environment (tech). LOOSE HOUSING SYSTEM: Positive correlations existed between behave and injury, and between tech and injury. Negative correlations were found between milk and cell, equal and tech, and milk and age. The magnitudes of these correlations were quantified by means of linear regression analysis. Comparison of the two husbandry systems revealed that while the loose housing systems is associated with significantly more problems related to tech, it is associated with significantly fewer problems related to injury. It seems that in this housing system cows are better able to avoid injury since they are allowed to move freely. No significant differences in behavior were found between the two husbandry systems. The present study shows the importance of proper technical design of housing environments, both in relation to animal welfare and to economic profitability.
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PMID:[The impact of suboptimal animal husbandry practices on animal health and economic profitability using the example of tie-in and loose housing system of dairy cattle]. 1063 25

Hereditary thrombocythaemia (HT) is an autosomal dominant disorder with clinical presentation and complications resembling sporadic essential thrombocythaemia (ET). Mutations in the thrombopoietin (TPO) gene causing overproduction of TPO and elevated TPO serum levels have been found previously in three families with HT. Here, we present evidence for genetic heterogeneity by demonstrating that HT in a Spanish and a US family is caused by genes other than TPO. Affected family members in both families had normal TPO serum levels. Genetic linkage analysis with TPO microsatellite markers excluded TPO as the disease gene in the Spanish HT family, and sequencing of the TPO gene revealed no mutations in the propositus of the US family. To test a role for MPL, the gene for the TPO receptor, we identified three single nucleotide polymorphisms (SNP) and a novel polymorphic CA microsatellite marker. By linkage analysis, we excluded MPL as the cause of HT in the Spanish family. Interestingly, mapping of the CA microsatellite marker to a region 40.5 kb upstream of MPL revealed the presence of sequences from the TIE gene, which encodes a tyrosine kinase receptor expressed on megakaryocytes and endothelial cells. Thus, MPL and TIE are in close physical proximity, and the CA microsatellite described here will be a useful genetic marker for both genes.
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PMID:Hereditary thrombocythaemia is a genetically heterogeneous disorder: exclusion of TPO and MPL in two families with hereditary thrombocythaemia. 1093 Sep 85

We recently have introduced the term vasculogenic mimicry to describe the unique ability of aggressive melanoma tumor cells to form tubular structures and patterned networks in three-dimensional culture, which "mimics" embryonic vasculogenic networks formed by differentiating endothelial cells. In the current study, we address the biological significance of several endothelial-associated molecules (revealed by microarray analysis) with respect to expression and function in highly aggressive and poorly aggressive human cutaneous melanoma cell lines (established from the same patient). In a comparative analysis, CD31 was not expressed by any of the melanoma cell lines, whereas TIE-1 (tyrosine kinase with Ig and epidermal growth factor homology domains-1) was strongly expressed in the highly aggressive tumor cells with a low level of expression in one of the poorly aggressive cell lines. Vascular endothelial (VE)-cadherin was exclusively expressed by highly aggressive melanoma cells and was undetectable in the poorly aggressive tumor cells, suggesting the possibility of a vasculogenic switch. Down-regulation of VE-cadherin expression in the aggressive melanoma cells abrogated their ability to form vasculogenic networks and directly tested the hypothesis that VE-cadherin is critical in melanoma vasculogenic mimicry. These results highlight the plasticity of aggressive melanoma cells and call into question their possible genetic reversion to an embryonic phenotype. This finding could pose a significant clinical challenge in targeting tumor cells that may masquerade as circulating endothelial cells or other embryonic-like stem cells.
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PMID:Expression and functional significance of VE-cadherin in aggressive human melanoma cells: role in vasculogenic mimicry. 1141 60

Ischemic preconditioning (IPC) of the brain describes the neuroprotection induced by a short, conditioning ischemic episode (CIE) to a subsequent severe (test) ischemic episode (TIE). Most of the supporting evidence for IPC is based on histological assessment, several days after TIE. The aim of this study is to investigate if changes induced by IPC can be detected within 30 min of reperfusion following the ischemic episode. A rat model of "four-vessel occlusion" transient global cerebral ischemia and parametric analysis of electrocorticogram were used. A control group was subjected directly to a 10 min TIE, and in a preconditioned group TIE was induced 48 h after a 3 min CIE. Quantitative histology was performed 48 h after TIE. Our key finding is that, 30 min after reperfusion, there is a significant increase in the electrocortical slow activity in the control group but not in the preconditioned group. Moreover the increase inversely correlates with the degree of electrocortical suppression during seconds 10 to 15 after the onset of the ischemic episode.
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PMID:Early electrocortical changes consistent with ischemic preconditioning in rat. 1216 90

A necessity for development and tumor progression is a blood supply formed by vasculogenic and/or angiogenic events, involving the cooperative interactions of cells with their microenvironment. Based on the recent characterization of vasculogenic mimicry by aggressive melanoma cells, particularly their ability to express VE (vascular endothelial)-cadherin, TIE-1, and EphA2, current studies have focused on the molecular signals deposited by these cells as they remodel their microenvironment. The experimental approach utilizes unique three-dimensional collagen matrices preconditioned by metastatic melanoma cells, which contain laminin 5 gamma2 chain-enriched tracks with promigratory cleavage fragments produced by cooperative interactions with specific matrix metalloproteinases (MMPs). The results demonstrate that the collagen matrices preconditioned by the metastatic cells induce poorly aggressive melanoma cells to express, for the first time, key angiogenic/vasculogenic/matrix-remodeling genes. Treatment of aggressive melanoma cells with an MMP inhibitor resulted in the inhibition of vasculogenic mimicry-associated genes in these tumor cells and abrogation of the inductive effects of the preconditioned matrix on poorly aggressive melanoma cells. These observations illustrate the remarkable influence of the microenvironment on the phenotype of melanoma cells and may provide new perspectives on tumor cell plasticity and unique treatment strategies.
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PMID:Remodeling of the microenvironment by aggressive melanoma tumor cells. 1281 47

We describe a patient, in whom giant liver hemangioma (GLH) was found by ultrasound study in screening for hypertension. Two of her sisters also had GLH. One of them had become symptomatic and the hemangioma was successfully removed. The other sisters were carefully watched. Our patient didn't need any intervention in 4 years of follow-up. The pathogenesis of GLH is still unknown. Recent investigations show a role of the TIE receptor/angiopoietin system in vascular malformations. In literature we only found two other reports about a familial occurrence of liver hemangiomas. A genetic defect in familial GLH has not yet been identified.
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PMID:Giant liver hemangioma in three sisters. 1474 87

A tethered imine-enamine methodology has been developed for the direct conversion of 1,2,4-triazines into highly substituted pyridines via the inverse electron demand Diels-Alder reaction which avoids the need for a discrete aromatisation step. This TIE methodology has also been applied in one pot reaction cascades involving 1,2,4-triazines and utilising MnO(2)-mediated tandem oxidation processes (TOPs).
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PMID:Highly substituted pyridines via tethered imine-enamine (TIE) methodology. 1497 81

Direct methods in real and reciprocal space are developed for structural reversion. The direct method in real space involves the use of a novel method to retrieve the phase in the image plane using transport of intensity equation/maximum entropy method (TIE/MEM) and exit wave reconstruction by self-consistent propagation. Since the exit wave is restored from the complex signal in the image planes, no image model between the exit wave and image is assumed. The structural information in the reconstructed exit wave is then further extended by a "complex" maximum entropy method as a direct method in reciprocal space to extrapolate the phase to higher frequencies.
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PMID:Resolution extension and exit wave reconstruction in complex HREM. 1504 90


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