Disease relevance of Anxa5

• The tumor suppressor gene candidate APRG1 was positioned close to the border of the homozygous deletion in a small cell lung cancer cell line ACC-LC5 [1].
• Detection of cardiomyocyte death in a rat model of ischemia and reperfusion using 99mTc-labeled annexin V [2].
• First, a mutant of annexin V was constructed with an N-terminal extension of six amino acids (Met-Ala-Cys-Asp-His-Ser) and with Cys316 mutated to Ser; this molecule was expressed in Escherichia coli [3].
• METHODS: We exposed cultured GENs to hypoxia and observed apoptosis by annexin V assay [4].
• Annexin V imaging may be useful clinically in the diagnosis and management of myelodysplastic syndrome [5].

High impact information on Anxa5

• These alterations in annexin V suggest a role for domain 3 in calcium-triggered interaction with phospholipid membranes [6].
• C5a blockade dramatically reduced thymocyte apoptosis as measured by thymic weight, binding of annexin V to thymocytes, and laddering of thymocyte DNA [7].
• Blocking of Fas protein reduced the number of apoptotic cells in the liver; binding of annexin V to phosphatidylserine (PS) reduced the number of PMNs phagocytosed by Kupffer cells [8].
• The presence of apoptosis was evaluated by morphological criteria, annexin V binding, and DNA fragmentation and quantified as the proportion of hypodiploid cells by flow cytometry [9].
• Thrombin activation was also seen with apoptotic human VSMCs (AUC of 211 +/- 8 nmol x min/L; PT of 103 +/- 4 nmol/L) and was inhibited by annexin V (P < .0001 for AUC and PT) [10].

Chemical compound and disease context of Anxa5

• CONCLUSION: Acute doxorubicin-induced cardiomyopathy based on early apoptosis can be assessed and imaged with annexin V scintigraphy in rats [11].
• The end points were percent infarction/risk zone and annexin-V (apoptosis) and/or propidium iodide positivity (necrosis), respectively [12].
• In nephritis, the lumen of distal tubules and the luminal cell membrane were deeply stained, with leakage of annexin V being observed from tubular cells [13].
• The effect of MPP+ on the morphology of C6 glioma cells was observed under phase contrast microscopy; apoptosis of C6 glioma cells were measured by FITC-labeled Annexin V staining and flow cytometry [14].

Biological context of Anxa5

• Here, we investigated in detail and correlated the adsorption kinetics of annexin A5 on SLBs, supported on silica and on mica, with the protein's 2D self-assembly behavior [15].
• Herein, we screened an embryonic day 17 rat brain cDNA library by western blot using glutathione S-transferase-annexin V fusion protein as a probe and then isolated four clones showing binding to annexin V in a Ca2+ - and phospholipid-dependent manner [16].
• Previous studies found that both human and chicken annexin V genes bear 13 exons and one promoter, which possess no TATA sequence or CCAAT box, and have a high GC content [17].
• We also demonstrated the presence of at least four species of rat annexin V transcripts that were generated by distinct transcription initiation and alternative splicing [17].
• We report here the isolation and characterization of the entire rat annexin V gene, which is shown to span about 40 kbp, and to consist of 14 exons, 13 introns and two promoters [17].

Anatomical context of Anxa5

• By immunohistochemistry, Anx 1 was detected only in the cytoplasm of hepatocytes of 1- to 3-day-old rats, Anx 2 and 6 both exhibited a redistribution from the cytoplasm toward the plasma membrane, and Anx 5 was present in the nucleus, cytoplasm, and plasma membrane [18].
• In the DRG, annexin V is expressed in relatively high concentrations in small sensory neurons in contrast to the SC, where it is expressed mainly by ependymal cells and by small-diameter axons located in the superficial laminae of the dorsal horn areas [19].
• These results show that Annexin V, a member of the calcium-dependent phospholipid binding proteins, is synthesized in the rat pituitary gland, and suggest its association with prolatin in the gland [20].
• Association of annexin V with prolactin in the rat anterior pituitary gland [20].
• TPO ameliorated DOX-induced apoptosis of H9C2 cells as demonstrated by assays of annexin V, active caspase-3, and mitochondrial membrane potential [21].

Associations of Anxa5 with chemical compounds

• In the present studies, site-directed mutagenesis was combined with x-ray crystallography and solution liposome binding assays to probe the functional role of a cluster of interfacial basic residues in annexin V [22].
• In the present study, the importance of tryptophan 185, and threonine or serine at positions 72, 144, 228, and 303, in rat annexin V is investigated by site-directed mutagenesis, X-ray crystallography, and functional assays [23].
• The assays indicate that relative to wild-type annexin V, loss of the methyl substituent at position 72 (Thr72-->Ser) has no effect while loss of the hydroxyl group (Thr72-->Ala or Thr72-->Lys) causes reduction of membrane binding [23].
• VEGF induced a rapid tyrosine phosphorylation of lipocortin V in human umbilical vein endothelial cells (HUVEC) [24].
• Liposomes containing phosphatidylserine but not phosphatidylinositol inhibited uptake of apoptotic cells in a dose-dependent manner to a maximum of 50% inhibition; annexin V also inhibited the uptake of apoptotic cells in a dose-dependent and calcium-dependent manner [25].

Regulatory relationships of Anxa5

• On the other hand, IL-15 failed to influence the increase in cell death after PI and annexin V staining [26].

Other interactions of Anxa5

• In contrast, camptothecin- and etoposide-induced killing is associated with robust increases in caspase 3 activation and annexin V staining [27].
• Cell death, presumably by apoptosis as evidence by TUNEL and Annexin V binding, was observed following LPS/IFN-gamma, progenitors being more sensitive than differentiated cells [28].
• Hyperosmolarity, however, sensitized hepatocytes toward CD95L-induced apoptosis, as assessed by annexin V staining and terminal deoxynucleotidyl transferase-mediated X-dUTP nick-end labeling (TUNEL) assay [29].
• Thymocytes obtained 2 or 3 h after CLP and exposed in vitro to C5a, but not normal thymocytes, underwent increased apoptosis, as demonstrated by annexin-V binding, coinciding with increased activation of caspases 3, 6, and 8 [30].
• Antibody was produced against the annexin consensus peptide, Lys-Ala-Met-Lys-Gly-Leu-Gly-Thr-Asp-Glu, which was derived from the sequence of several Ca2+/phospholipid-binding proteins including calpactin, lipocortin, endonexin II, 67-kDa calelectrin, lymphocyte 68-kDa protein, and protein II [31].

Analytical, diagnostic and therapeutic context of Anxa5

• Molecular cloning and characterization of annexin V-binding proteins with highly hydrophilic peptide structure [16].
• The existence of Annexin V mRNA in rat pituitary glands was also confirmed by polymerase chain reaction [20].
• Co-immunoprecipitation of translated proteins confirmed the interaction between the VEGF receptor and lipocortin V [24].
• DNA replication was determined by incorporation of bromodeoxyuridine and apoptosis by the annexin V binding and terminal deoxynucleotidyl transferase-mediated dUTP-X nick end labeling (TUNEL) assays [32].
• Granulocytes in cultures that contained 2.4G2 showed chromatin condensation, binding of Annexin-V, and fas induction, and by electron microscopy, apoptosis was most commonly observed in cells of the eosinophil lineage [33].

References