Disease relevance of ATF7IP

• Altered MCAF expression can therefore enhance the ability of activated monocytes to kill brain tumor cells [1].
• Cachexia-inducing adenocarcinoma cells (cell line colon 26, clone 20) were transfected with either a control plasmid or MCAF expression vector [2].
• To evaluate the effect of monocyte chemotactic and activating factor (MCAF/MCP-1/JE) on tumor progression and metastasis [2].
• We report the novel finding that psoriasis has strong positive immunostaining for MCAF located to all the layers of the epidermis, except the stratum granulosum, in pustular, guttate and chronic plaque psoriasis [3].
• Preincubation of basophils with pertussis toxin markedly diminished the basophil response to either RANTES or MCAF/MCP-1 [4].

High impact information on ATF7IP

• Recombinant monocyte chemotactic-activating factor (MCAF) has been shown to induce histamine release from human basophils with a dose response between 10(-9) and 10(-6) M [5].
• However, interleukin 3 (IL-3) and IL-5 could each prime basophils for MCAF-induced secretion [5].
• At a suboptimal concentration (2.5 x 10(-9) M), MCAF was unable to prime the basophil to histamine release by other secretagogues [5].
• Our findings suggest that MCAF may contribute to the accumulation of macrophages in inflamed rheumatoid joints [6].
• These results suggest that RANTES and MCAF/MCP-1: 1) are potent activators of basophils; 2) may function via the same, or a closely related, receptor system in basophils; and 3) may represent a link between activation of monocytes, lymphocytes, and basophils in inflammatory disorders such as the late phase allergic reaction [4].

Biological context of ATF7IP

• The results of RT-PCR analysis indicated that haemodialysis stimulates the gene expression of MCAF in PBMC in vivo [7].
• Transfection of MCAF expression vector did not affect the growth rate in vitro [2].
• The production of MCAF reached 0.4 ng/ml in vitro when transfectant cells were cultured at a cell density of 5 x 10(4) cells/ml for 3 days [2].
• Recombinant human monocyte chemotactic and activating factor (MCAF) was iodinated and specific binding sites for this cytokine were detected on human peripheral blood monocytes, the monocytic leukemia cell line THP-1, and on PMA-differentiated HL60 and U937 cell lines [8].
• Blocking studies demonstrated that a rabbit polyclonal antibody to monocyte chemotaxis and activating factor (MCAF) inhibited all monocyte chemotaxis by greater than 80% [9].

Anatomical context of ATF7IP

• PURPOSE: In order to evaluate the possibility of synergistic antitumor gene therapy by the gene delivery of monocyte chemotactant protein-1 (MCP-1/MCAF/IE), the effect of a biological response modulater for macrophages on tumor progression of gene transfected tumor cells was studied [10].
• Immunoreactive cells of MCAF/MCP-1 were also stained with the antibody, which recognizes monocytes and macrophages [11].
• DESIGN: Detection of MCAF/MCP-1 in culture supernatants of nasal mucosa using Western blot analysis and assay of histamine release from basophils induced by these culture supernatants [11].
• Detection of MCAF/MCP-1 expression in nasal mucosa of patients with perennial allergic rhinitis using immunohistochemistry [11].
• Endothelial cells, renal epithelial cells and infiltrating mononuclear cells in the tubulointerstitial regions were MCAF-positive in immunohistochemical as well as in situ hybridization analysis [12].

Associations of ATF7IP with chemical compounds

• Urinary MCAF levels in the patients with active lesions were significantly higher than those with inactive lesions (20.3 +/- 6.4 vs. 1.7 +/- 0.3 pg/ml . creatinine, P < 0.01) [12].
• Incubation with cycloheximide did not block the rapid reappearance of MCAF receptors within 20 min on the cell surface indicative of receptor recycling rather than new protein synthesis [8].
• Northern blot analysis using enzyme inhibitors showed that phospholipase C, protein kinase C, and tyrosine kinase were involved in the stretch-induced gene expression of IL-8 and MCAF/MCP-1, whereas cAMP- or cGMP-dependent protein kinase was not [13].
• Monocytes stimulated with PPD or M. tuberculosis expressed low levels of antigenic interleukin-8 but high levels of MCAF/MCP-1 compared with monocytes stimulated with lipopolysaccharide [14].
• These findings suggest that MCAF, alone or in concert with other cytokines, primes monocytes for enhanced release of 02-, and that MCAF- or FMLP-induced intracellular acidification and alkalinization are closely associated with an increase in [Ca2+]i, but not O2- release [15].

Regulatory relationships of ATF7IP

• Selective depletion of MCAF1 or Sp1 down-regulates TERT and TERC genes in cultured cells, which results in decreased telomerase activity [16].

Analytical, diagnostic and therapeutic context of ATF7IP

• The levels of MCAF/MCP1 (mean +/- S.E.M.) were 107 +/- 15.8 pg/ml in patients with AA, 393.4 +/- 105.9 pg/ml in CHB and 36.4 +/- 10.9 pg/ml in the control group (P < 0.05) [17].
• The aim of the current study was to examine associations among MCAF/MCP1 and bronchoalveolar lavage fluid (BALF) cells and disease severity as measured by airway caliber and bronchial hyperresponsiveness in patients with AA and CHB [17].
• METHODS: Plasma levels of MCAF were determined by ELISA [7].
• IL-1-treated HEC expressed high levels of MCAF/MCP-1/TDCF mRNA transcripts, as assessed by Northern blot analysis [18].
• The purified MCAF showed microheterogeneity yielding two bands on SDS-PAGE analysis [19].

References