Disease relevance of ATP8A2

• The oncogene c-myb, which is specifically expressed and regulated in hematopoietic cells, was found to be amplified in cell lines ML-1, ML-2, and ML-3, which were separately cultured from cells of a patient with acute myelogenous leukemia (AML) [1].
• Here we show that vaccinia topoisomerase, a eukaryotic type IB enzyme, catalyzes site-specific endoribonucleolytic cleavage of an RNA-containing strand [2].
• Highlights are the chromosomal localization of at least five genes for autosomal forms of non-syndromic deafness and, more recently, the cloning of an X-linked deafness gene, DFN3, and the Usher syndrome type IB gene [3].
• This report describes a gene, MCL1, that we isolated from the ML-1 human myeloid leukemia cell line during phorbol ester-induced differentiation along the monocyte/macrophage pathway [4].
• To investigate the mechanism for lineage-specific toxicity, the effects of ara-G were compared in CEM (T-lymphoblast), Raji (B-lymphoblast), and ML-1 (myeloid) cell lines [5].

High impact information on ATP8A2

• We have now purified a DIF to homogeneity from medium conditioned by PHA-stimulated leukocytes using a human myeloblastic leukemia cell line, ML-1, as target cells [6].
• The expression of the 63D3-defined antigen was also markedly augmented in the ML-1, KG-1, and THP-1-0 cells, but it was not significantly altered in the HL-60 cells [7].
• Furthermore, a dynamic expression profile for the BMP receptor (BMPR) isoform IB was observed, with dramatic up-regulation during osteogenesis [8].
• Osteogenic differentiation of mouse adipose-derived adult stromal cells requires retinoic acid and bone morphogenetic protein receptor type IB signaling [8].
• Phospholamban domain IB forms an interaction site with the loop between transmembrane helices M6 and M7 of sarco(endo)plasmic reticulum Ca2+ ATPases [9].

Chemical compound and disease context of ATP8A2

• To elucidate the differentiation-associated expression of enzymes catalyzing arachidonic acid metabolism, we measured arachidonate metabolites by reverse-phase high pressure liquid chromatography in monocytoid leukemia (ML-1, THP-1, and U937) and myeloid leukemia (KG-1) cell lines [10].
• Two recently derived human myeloid leukemia cell lines, ML-1 and ML-2, were induced to differentiate by treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) or with retinoic acid for 5 to 12 days [11].
• N-Trifluoroacetyladriamycin-14-O-hemiadipate (AD 143), a DNA nonbinding derivative of Adriamycin, was studied for its effect on the uptake of labeled nucleosides into human leukemia (ML-1) and lymphoma (P3HR-1) cells in culture [12].
• We have shown that 1-(5-chloronaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine hydrochloride (ML-9), an inhibitor of myosin light chain kinase, induces differentiation of monocytoid leukemia cell lines U937 and THP-1 but not of myeloblastic leukemic ML-1 cell or erythroleukemia K562 cells [13].
• The theory has been tested on human myeloid leukemia cells (line ML-1) in which membrane potential changes were induced by valinomycin clamping in various K+ gradients [14].

Biological context of ATP8A2

• The ML-1 gene has a DNA sequence that is 2177 bp in size and is located on chromosome number 13 on the q arm at site 12-14 [15].
• Changes in levels of normal ML-1 gene transcripts associated with the conversion of human nontumorigenic to tumorigenic phenotypes [15].
• By restriction endonuclease digestion and hybridization with cloned heavy chain immunoglobulin gene probes for the constant (Cmu) and joining (JH) regions, the DNA of 2 patients and 1 cell line (ML-1) was found to contain rearrangements [16].
• A partially purified fraction from pokeweed mitogen-stimulated human leukocyte-conditioned medium which effectively induced ML-1 cell differentiation also prevented the down modulation of PDB receptors [17].
• Cytogenetic studies were performed on ML cell lines (ML-1, -2, and -3), as well as on the leukemic cells of a patient from whom the ML cells were derived [18].

Anatomical context of ATP8A2

• These other human cells include adherent monocytes and the cell line ML-1, which can be induced to differentiate along the monocyte-macrophage pathway [19].
• Monocyte nonspecific esterase has been purified from cultured cells of the acute myeloid leukemia cell line, ML-1 [20].
• DNA-specific agents have the capacity to induce the maturation of ML-1 human myeloblastic leukemia cells to monocyte/macrophages if adequate concentrations of fetal bovine serum or mitogen-stimulated human leukocyte-conditioned medium (CM) are present in the culture medium [21].
• The ML cell lines (ML-1, -2, and -3) were derived from the cells of a patient with T-cell malignant lymphoma who developed acute myeloblastic leukemia and whose cells showed a primary chromosome change at band 11q24 [22].
• In contrast, under serum-free conditions, medium conditioned by phytohemagglutinin-stimulated leukocytes promoted the clonal growth of both ML-1 and HL-60 cells at the lower concentrations [23].

Associations of ATP8A2 with chemical compounds

• All the COX metabolites were elevated, but thromboxane A2 (TXA2) formation was threefold higher in ML-1 cells than in THP-1 cells [10].
• Increased COX metabolite formation in differentiated THP-1 and ML-1 cells was due to an enhanced level of prostaglandin H synthase enzyme mass, as measured by Western blot analysis [10].
• After preincubation with AD 143 at concentrations as low as 5.2 microM (ML-1) or 13 microM (P3HR-1), the ability of the cells to take up extracellular labeled nucleosides was decreased by more than 50% [12].
• Differentiation-uninduced ML-1 cells do not respond to treatment with N-nitroso-N-methylurea, indicating that differentiation-induced cells, at an early stage of the maturation process, may be the targets for the carcinogen-mediated transformation [24].
• To examine the mechanism by which this interactive effect occurs, ML-1 cells were exposed to actinomycin D or daunomycin in various combinations with CM, using concentrations at which neither the drug nor CM, when applied individually, induced maturation to a significant extent [21].

Analytical, diagnostic and therapeutic context of ATP8A2

• Kinetics of appearance of differentiation-associated characteristics in ML-1, a line of human myeloblastic leukemia cells, after treatment with 12-O-tetradecanoylphorbol-13-acetate, dimethyl sulfoxide or 1-beta-D-arabinofuranosylcytosine [25].
• The human cyclin A1 is specifically expressed in testis and brain among all of the normal tissues that we studied by Northern blot analysis; in addition, it is expressed in several myeloid leukemia cell lines, including ML-1, U937, NB4, KG-1, and THP1 [26].
• Using a reverse transcriptase-polymerase chain reaction procedure (RT-PCR), we found a transcript corresponding to sequences upstream of the VH6 promoter in RNA from both the lymphoblastoid cell line ML-1, which actively transcribes the VH6 promoter, and the REH cell line, which does not [27].
• A human placenta cDNA library was screened and PCR of brain, placenta, and lymphocyte cDNAs was performed in order to isolate the human alpha1,2-mannosidase IB cDNA [28].
• Subsequent sequence analysis revealed that PLA(2) clones encoding group IB" PLA(2) [29].

References