Disease relevance of Anxa1

• Molecular cloning and expression in Escherichia coli of the cDNA coding for rat lipocortin I (calpactin II) [1].
• Microvilli isolated from the MAT-C1 ascites subline of the 13762 rat mammary adenocarcinoma contain a major calcium-sensitive microfilament-binding protein, AMV-p35 (ascites microvillar p35) [2].
• Here, the levels of two calpain-specific substrates, p35 protein and eukaryotic initiation factor 4G (eIF4G), as well as its physiological regulator calpastatin, were investigated in a rat model of transient global cerebral ischemia with or without ischemic tolerance (IT) [3].
• In rats without IT, the p35 levels slightly decreased after ischemia or reperfusion, whereas the levels of p25 (the truncated form of p35) were much higher than those in sham control rats after ischemia and remained elevated during reperfusion [3].
• The mean mRNA ratio of annexin-I/GAPDH was increased in liver tissue by 115% (P < 0.05) but unchanged in kidney tissue following induction of cirrhosis [4].

High impact information on Anxa1

• The cdk5/p35 kinase is essential for neurite outgrowth during neuronal differentiation [5].
• A similar extent of neurite outgrowth inhibition was obtained by transfection of an antisense p35 construct, which in turn was only rescued by p35 but not cdk5 coexpression [5].
• Here we show that both cdk5 and p35 proteins are present in the growth cones of developing neurons [5].
• The protein content of annexin-I and -V were not affected by bile duct excision in liver and kidney tissue indicating that upregulation of group II PLA2 activity was not due to downregulation of annexin-I or -V [4].
• Monoclonal antibodies were produced that recognize a membrane protein of 35,000 Da (p35) expressed in brain and adrenal medulla [6].

Chemical compound and disease context of Anxa1

• Specifically, the effects of domoic acid excitotoxicity can be alleviated only with crmA, p35 and gamma34.5 whereas all genes tested can protect against heat stress [7].

Biological context of Anxa1

• Thus upregulation of PLA2 enzyme and downregulation of lipocortin-I might account for the enhanced inflammatory response in hypoglucocorticoid states [8].
• A cDNA coding p35 was isolated from a rat brain cDNA library by immuno-screening, and the primary structure of the protein was revealed to be identical to that of HPC-1 (Inoue, A., Obata, K., and Akagawa, K. (1992) J. Biol. Chem. 267, 10613-10619) [6].
• Moreover, when the isolated islets were stimulated by a high concentration of glucose (20 mM), the phosphorylation of annexin-I was markedly enhanced, and it was synchronized to insulin secretion [9].
• Annexin-I regulation in response to suckling and rat mammary cell differentiation [10].
• Expression of annexin-I was investigated in the rat mammary gland during pregnancy, lactation, and involution [10].

Anatomical context of Anxa1

• In adult hepatocytes cultured in the presence of EGF or HGF, Anx 1 and 2 expressions resumed [11].
• Involvement of annexin-I in glucose-induced insulin secretion in rat pancreatic islets [9].
• Immunoelectron microscopic analysis of pancreatic beta-cells demonstrated that immunogold particles reactive to annexin-I were almost exclusively observed on most of the insulin-containing granules (approximately 90%) and less frequently located in cytosol and other organelles, such as the endoplasmic reticulum and mitochondria [9].
• A co-immunoprecipitation study indicated the in vivo association between Cdk5 and p35 in both DRG and sciatic nerve [12].
• The property of calcium-dependent binding of lipocortin to the particulate fraction was used to prepare cytosolic and particulate subcellular fractions which contained phospholiphase A2 activity but no lipocortin-I [13].

Associations of Anxa1 with chemical compounds

• Prenatal administration of dexamethasone (dex) resulted in a decrease of Anx 1 mRNA levels, and a strong increase in Anx 2 mRNA contents [11].
• The number of annexin-I gold particles located on insulin granules after oral glucose administration was significantly increased compared with that observed in fasted rats [9].
• BACKGROUND: EPC-K1, a diester of alpha-tocopherol and ascorbic acid, has a hydroxyl radical scavenging effect and also has antiinflammatory properties through its phospholipase A2 inhibitory effect [14].
• Immunoreactive calpactin II, a well-known substrate for EGF-receptor kinase, was found predominantly in the cytosol, although a second immunoreactive pool was found in a Triton X-100-extractable membrane fraction [15].
• Western blot analysis revealed no appreciable change in the expression of Cdk5 protein levels while, its regulatory proteins, p35 and p67 showed decreased levels following chronic ethanol treatment [16].

Regulatory relationships of Anxa1

• Annexin-I inhibits PMA-induced c-fos SRE activation by suppressing cytosolic phospholipase A2 signal [17].
• Epidermal growth factor induces the accumulation of calpactin II on the cell surface during membrane ruffling [15].

Other interactions of Anxa1

• Differential localization of calmodulin, the 67kDa calcimedin and calpactin II in secretory ameloblasts [18].

Analytical, diagnostic and therapeutic context of Anxa1

• Although IT did not promote significant changes in p35 and p25 levels, it induced a slight increase in calpastatin and eIF4G levels in the hippocampal subregions after 4 h of reperfusion [3].
• The mRNA of PLA2(group I and II) and annexin-I a presumptive inhibitor of PLA2 enzyme was measured by PCR using glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as an internal standard [4].
• The decrease in lipocortin-I mRNA in ADX rats was reflected by a corresponding decrease in tissue (lung, spleen, liver, and kidney) lipocortin-I protein content, as assessed by quantitative Western blot analysis [19].
• Adrenalectomy decreases lipocortin-I messenger ribonucleic acid and tissue protein content in rats [19].
• Immunoprecipitations of membrane-bound calpactin II from 32P-labeled cells indicate a transient EGF-dependent phosphorylation of calpactin II correlating with membrane ruffling [15].

References