Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice - Wikidata - awgldk - TriplyDB

Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

http://www.wikidata.org/entity/Q28344139

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Megsin gene: its genomic analysis, pathobiological functions, and therapeutic perspectives An Update on the Use of Animal Models in Diabetic Nephropathy Research Advanced glycation end products and diabetic complications Advanced Glycation End Products, Diabetes, and Bone Strength Identification of mouse orthologue of endogenous secretory receptor for advanced glycation end-products: structure, function and expression The multiple faces of RAGE--opportunities for therapeutic intervention in aging and chronic disease [Protein glycation as a pathological mechanism in diabetes].Dangers within: DAMP responses to damage and cell death in kidney disease.Advanced glycation end products induce tubular epithelial-myofibroblast transition through the RAGE-ERK1/2 MAP kinase signaling pathway Molecular mechanisms of diabetic vascular complications Controlling the receptor for advanced glycation end-products to conquer diabetic vascular complications S100B and APP promote a gliocentric shift and impaired neurogenesis in Down syndrome neural progenitors.Deletion of the receptor for advanced glycation end products reduces glomerulosclerosis and preserves renal function in the diabetic OVE26 mouse.Effect of circulating soluble receptor for advanced glycation end products (sRAGE) and the proinflammatory RAGE ligand (EN-RAGE, S100A12) on mortality in hemodialysis patients Paradoxical function for the receptor for advanced glycation end products in mouse models of pulmonary fibrosis.Activation of bone morphogenetic protein 4 signaling leads to glomerulosclerosis that mimics diabetic nephropathy Establishment of a diabetic mouse model with progressive diabetic nephropathy.Glomerular proteinuria: a complex interplay between unique players.Regulation of RAGE for attenuating progression of diabetic vascular complications.Bone fragility in type 2 diabetes mellitus.Tuberculosis susceptibility of diabetic mice.Alagebrium reduces glomerular fibrogenesis and inflammation beyond preventing RAGE activation in diabetic apolipoprotein E knockout mice ATP synthase subunit-β down-regulation aggravates diabetic nephropathy.Role of advanced glycation end products and their receptors in development of diabetic neuropathy.Synergistic contributions of carbonyl stress and megsin in diabetic nephropathy.Advanced glycation end product receptor-mediated cellular dysfunction.Can advanced glycation end product inhibitors modulate more than one pathway to enhance renoprotection in diabetes?The association between interleukin-19 concentration and diabetic nephropathy.Role of the JAK/STAT signaling pathway in diabetic nephropathy.A novel function of the receptor for advanced glycation end-products (RAGE) in association with tumorigenesis and tumor differentiation of HCC Vascular complications of diabetes: mechanisms of injury and protective factors Specific siRNA targeting receptor for advanced glycation end products (RAGE) decreases proliferation in human breast cancer cell lines.Receptor for advanced glycation end products (RAGE) deficiency attenuates the development of atherosclerosis in diabetes.sRAGE induces human monocyte survival and differentiation Markers of glycemic control in the mouse: comparisons of 6-h- and overnight-fasted blood glucoses to Hb A1c.Advances in murine models of diabetic nephropathy.Reducing cardiovascular events in high-risk patients: the challenge of managing hypertension in patients with diabetic renal disease.Spontaneous bone loss in RIP-iNOS transgenic mouse: a mouse model for diabetes-mediated osteopenia/osteoporosis.Receptor for AGEs (RAGE) blockade may exert its renoprotective effects in patients with diabetic nephropathy via induction of the angiotensin II type 2 (AT2) receptor.Bone metabolism and fracture risk in type 2 diabetes mellitus.

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P2860

Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

http://www.wikidata.org/entity/Q28344139

description

2001 nî lūn-bûn

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2001 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2001年の論文

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2001年論文

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2001年論文

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2001年論文

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2001年論文

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2001年論文

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2001年论文

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name

Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

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Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

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Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

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Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

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Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

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Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

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Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

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Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

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Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

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Journal of Clinical Investigation

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Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

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H Okamoto

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H Yamamoto

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H Yonekura

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M Takeuchi

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P2860

RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides

Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins

A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding

Three genes in the human MHC class III region near the junction with the class II: gene for receptor of advanced glycosylation end products, PBX2 homeobox gene and a notch homolog, human counterpart of mouse mammary tumor gene int-3

The S100 family of EF-hand calcium-binding proteins: functions and pathology

The receptor for advanced glycation end products (RAGE) is a cellular binding site for amphoterin. Mediation of neurite outgrowth and co-expression of rage and amphoterin in the developing nervous system

Glomerulosclerosis in mice transgenic for growth hormone. Increased mesangial extracellular matrix is correlated with kidney mRNA levels.

Microalbuminuria, blood pressure and diabetic renal disease: origin and development of ideas.

Advanced glycosylation end products in tissue and the biochemical basis of diabetic complications.

Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues.

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