Disease relevance of Nme2

• The cDNAs of nm23-M1, nm23-M2, and a combination of both were transfected into the highly metastatic melanoma subline FE7, with low nm23 expression [1].
• The number of pulmonary metastases developed by these sublines was inversely correlated with the expression of two isotypes of nm23, nm23-M1 and nm23-M2 [1].
• Recently, the nm23-M2 locus was identified as a common leukemia retrovirus integration site, suggesting that it plays a role in leukemia development [2].
• Identification by array screening of altered nm23-M2/PuF mRNA expression in mouse retinal degeneration [3].
• We have analyzed one such peptide, P18 from the V3 loop of HIV-1 gp160, which we have previously shown to be recognized by CD8+ CTL with the class I molecule H-2Dd, and by CD4+ Th cells with the class II molecule I-Ad [4].

Psychiatry related information on Nme2

• Response latencies and interpeak intervals matured rapidly over the course of the second and third postnatal weeks and did not achieve adultlike characteristics until after P18 [5].

High impact information on Nme2

• Between P18 and P35, there was an increase in two biomarkers of oxidative damage, carbonyl adducts measured by ELISA and immunohistochemical staining for acrolein, in the retinas of rd1 mice [6].
• Spleen cells from vaccinia-infected control mice displayed strong CD8+ cytolytic activity against gp160-transfected fibroblasts and fibroblasts pulsed with a peptide (P18) representing a CTL epitope of gp160 [7].
• Two isotypes of murine nm23/nucleoside diphosphate kinase, nm23-M1 and nm23-M2, are involved in metastatic suppression of a murine melanoma line [1].
• Factor-induced expression of nm23-M2 was regulated specifically at the level of polysome association by a phosphoinositide 3-kinase-dependent mechanism [2].
• The putative proto-oncogene nucleoside diphosphate kinase B (ndpk-B or nm23-M2) was identified as an erythropoietin and stem cell factor target gene [2].

Chemical compound and disease context of Nme2

• We detected altered expression of the gene encoding nm23-M2, a member of the family of nucleoside diphosphate kinases implicated in diverse processes including metastasis suppression and transcriptional regulation [3].
• We observed that longer versions of P18 and the murine cytomegalovirus pp89-derived core peptide, pMCMV, which could stimulate T cell hybridomas in FCS, were not as sensitive to the ACE inhibitor captopril as P18 [8].
• At P18, 7 days after the cessation of hypoxia, there was a marked increase in astroglial cell proliferation within the SVZ, as assessed by 5-bromodeoxyuridine (BrdU) incorporation in S-phase cells [9].

Biological context of Nme2

• In contrast nm23-M2 mRNA was shown to be more widely expressed.The relationship between nm23-M1 gene tissue-specific expression and the putative binding element of the promoter region is discussed [10].
• Identification of the transcription initiation site revealed that nm23-M2 mRNA starts with a terminal oligopyrimidine sequence, which is known to render mRNA translation dependent on mitogenic factors [2].
• Interestingly, stable transfection of the nm23-M2/NDPK-B del-RGD or G106A mutant gene in JB6 Cl 41-5a cells selectively abrogated NDPK-B-induced cellular transformation, implicating a possible Arg105-Gly106-Asp107 regulatory role in early skin carcinogenesis [11].
• We have studied the TCR V beta chain expression in CTL lines, either cross-reactive for these two peptides or specific for P18 alone, in these four different MHC haplotypes [12].
• The kinetics of the generation of T cell stimulatory activity among P18 variant peptides in serum differed with peptide length, and with the nature of amino and COOH-terminal extensions [8].

Anatomical context of Nme2

• Furthermore, a similar pattern of expression was described in the central nervous system for nm23-M2 mRNA, encoding a second isoform of the nucleoside diphosphate kinase [13].
• We have previously described a T cell hybridoma, A.1.1, that responds to specific Ag (P18, a synthetic polypeptide of defined sequence) in the context of I-Ad by producing lymphokines [14].
• These suppressor cells were active in inhibiting anti-SRBC responses in the absence of P18 and bore the Ly-2 surface marker [14].
• Oligonucleotide microarrays were used to compare gene expression profiles in the brainstem and thalamus of Sod2+/+ and -/- mice from birth to P18 [15].
• Abnormal cells were seen in the outer nuclear layer on P10 and among photoreceptors on P14; by P18 there were cell aggregates in the subretinal space with evidence of lumen formation [16].

Associations of Nme2 with chemical compounds

• Whole mounts of retinas perfused with fluorescein-labeled dextran showed a similar sequence of events, with sprouts from retinal vessels in the deep capillary bed seen on P14 and vessels reaching the subretinal space by P18 [16].
• These results suggest that a proline kink in alpha-helical antibiotic peptide P18 serves as a hinge region to facilitate ion channel formation on bacterial cell membranes and thus plays an important role in providing high selectivity against bacterial cells [17].
• Cocaine treatment elicited expression in control mice at P10 through P18 but not at P4 and P6 [18].
• The dynamics of dopamine receptor signaling efficacy were characterized in developing mice by measuring striatal c-Fos expression after dopaminergic agonist treatment at postnatal day 4 (P4) to P18 [18].
• Finally, using a low-affinity AMPA receptor antagonist (gamma-D-glutamylglycine), we show that desensitization occurs at P8-P10 but is absent at P16-P18, even during trains of high-frequency (100-300 Hz) stimulation [19].

Other interactions of Nme2

• Organization and expression of mouse nm23-M1 gene. Comparison with nm23-M2 expression [10].
• When the murine melanoma cell line was cotransfected with a nm23-M2/ NDP kinase expression vector and c-myc CAT, CAT activity was elevated [20].

Analytical, diagnostic and therapeutic context of Nme2

• Moreover, in situ hybridization also displayed a specific nuclear localization for nm23-M2 mRNA [21].
• Molecular cloning and functional expression of the second mouse nm23/NDP kinase gene, nm23-M2 [22].
• The same viral suspension was also injected sub-retinally into rhodopsin-knockout rho (-/-) mice either at P18 or P78, and retinas were analyzed by immunohistochemistry and PNA lectin histochemistry two weeks later [23].
• Western blot analysis showed that all the processing events occurred inside parasitized erythrocytes at the stage just prior to the schizont rupture, that P47 was further processed into two 25 kDa fragments and that the two fragments, which were linked to P18 through disulfide bonds, were associated with the merozoite [24].

References