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Gene Information
Gene symbol: ALB
Gene name: albumin
HGNC ID: 399
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | BCS1L | 1 hits |
| 2 | FOS | 1 hits |
| 3 | MAPK1 | 1 hits |
| 4 | MAPK10 | 1 hits |
| 5 | PRKCA | 1 hits |
| 6 | PTPRO | 1 hits |
| 7 | TGFB1 | 1 hits |
| 8 | TJP1 | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 3602581 | Samples of Bowman capsular space (BCS) obtained by free-flow renal micropuncture techniques with pressure control were analyzed for albumin and high-molecular-weight (HMW) proteins by ultramicrodisc electrophoresis. |
| 2 | 3602581 | The measured mean albumin and HMW protein concentration in BCS were 1.72 g/l and 0.66 g/l, respectively. |
| 3 | 3602581 | Samples of Bowman capsular space (BCS) obtained by free-flow renal micropuncture techniques with pressure control were analyzed for albumin and high-molecular-weight (HMW) proteins by ultramicrodisc electrophoresis. |
| 4 | 3602581 | The measured mean albumin and HMW protein concentration in BCS were 1.72 g/l and 0.66 g/l, respectively. |
| 5 | 10703671 | Results document that spontaneous proteinuria in MWF rats develops without significant changes in the permeability of the GBM to water and albumin, or in the ultrastructure of the podocyte foot processes, but is associated with an important alteration in the distribution of ZO-1 at the glomerular level. |
| 6 | 10703671 | Thus, renoprotective effects of ACE inhibitors are not associated with changes in intrinsic functional properties of GBM, or ultrastructural changes of the epithelial cells, but rather with preservation of glomerular ZO-1 distribution and slit diaphragm function, which are essential for maintaining the filtration barrier. |
| 7 | 11086029 | Reduced filtration surface area in association with these structural changes was confirmed by finding reduced glomerular nephrin content and reduced glomerular filtration rate in Ptpro(-/-) mice. |
| 8 | 11086029 | There was no detectable increase in the urine albumin excretion of Ptpro(-/-) mice. |
| 9 | 11576932 | In mesangial and endothelial cells, the AGE-RAGE interaction caused enhanced formation of oxygen radicals with subsequent activation of nuclear factor-kappaB and release of pro-inflammatory cytokines (interleukin-6, tumor necrosis factor-alpha), growth factors (transforming growth factor-beta1 [TGF-beta1], insulin-like growth factor-1), and adhesion molecules (vascular cell adhesion molecule-1, intercellular adhesion molecule-1). |
| 10 | 11576932 | In tubular cells, incubation with AGE albumin was followed by stimulation of the mitogen-activating protein (MAP) kinase pathway and its downstream target, the activating protien-1 (AP-1) complex, TGF-beta1 overexpression, enhanced protein kinase C activity, decreased cell proliferation, and impaired protein degradation rate, in part caused by decreased cathepsin activities. |
| 11 | 11576932 | The pathogenic relevance of AGEs was further verified by in vivo experiments in euglycemic rats and mice by the parenteral administration of AGE albumin, leading in the glomeruli to TGF-beta1 overproduction, enhanced gene expression of ECM proteins, and morphological lesions similar to those of DN. |
| 12 | 11576932 | In mesangial and endothelial cells, the AGE-RAGE interaction caused enhanced formation of oxygen radicals with subsequent activation of nuclear factor-kappaB and release of pro-inflammatory cytokines (interleukin-6, tumor necrosis factor-alpha), growth factors (transforming growth factor-beta1 [TGF-beta1], insulin-like growth factor-1), and adhesion molecules (vascular cell adhesion molecule-1, intercellular adhesion molecule-1). |
| 13 | 11576932 | In tubular cells, incubation with AGE albumin was followed by stimulation of the mitogen-activating protein (MAP) kinase pathway and its downstream target, the activating protien-1 (AP-1) complex, TGF-beta1 overexpression, enhanced protein kinase C activity, decreased cell proliferation, and impaired protein degradation rate, in part caused by decreased cathepsin activities. |
| 14 | 11576932 | The pathogenic relevance of AGEs was further verified by in vivo experiments in euglycemic rats and mice by the parenteral administration of AGE albumin, leading in the glomeruli to TGF-beta1 overproduction, enhanced gene expression of ECM proteins, and morphological lesions similar to those of DN. |