Disease relevance of Mixl1

• The effect of recombinant human interleukin-6 (rhIL-6) on induction of nitrite (NO(-2)) production was investigated in a mouse myeloid leukemia cell line (M1) and a subclone (Mm1) [1].
• Antibody-mediated enhancement of dengue virus infection in mouse macrophage cell lines, Mk1 and Mm1 [2].
• Mml loci have been identified as provirus integration sites among a subset of monocytic tumours induced by murine leukaemia virus (MuLV) infection of BALB/c and DBA/2 mice [3].

High impact information on Mixl1

• Enforced expression of Mixl1 profoundly perturbed hematopoietic lineage commitment and differentiation, giving rise to abnormal myeloid progenitors and impairing erythroid and lymphoid differentiation [4].
• To assess the role of Mixl1 in the regulation of adult hematopoiesis, we overexpressed Mixl1 in murine bone marrow using a retroviral transduction/transplantation model [4].
• Mixl1, the sole murine homologue of the Xenopus Mix/Bix family of homeobox transcription factors, is essential for the patterning of axial mesendodermal structures during early embryogenesis [4].
• Gene targeting and overexpression studies have implicated Mixl1 as a regulator of hematopoiesis arising in differentiating embryonic stem cells [4].
• The observation that the endoderm cells are inherently unable to move despite the expansion of the mesoderm in the Mixl1-null mutant suggests that the movement of the endoderm and the mesoderm is driven independently of one another [5].

Biological context of Mixl1

• To examine the role of Mixl1 in murine embryogenesis, we used gene targeting to create mice bearing a null mutation of Mixl1 [6].
• The primitive streak gene Mixl1 is required for efficient haematopoiesis and BMP4-induced ventral mesoderm patterning in differentiating ES cells [7].
• Mixl1 is required for axial mesendoderm morphogenesis and patterning in the murine embryo [6].
• The homeobox gene Mixl1 is expressed in the primitive streak of the gastrulating embryo, and marks cells destined to form mesoderm and endoderm [7].
• These sugars also blocked the phagocytosis of QRC by Mm1 cells but had no effect on either Fc-mediated phagocytosis or latex ingestion [8].

Anatomical context of Mixl1

• These data indicated that Mixl1 was required for efficient differentiation of cells from the primitive streak stage to blood [7].
• Mixl1 is therefore required for the morphogenesis of axial mesoderm, the heart and the gut during embryogenesis [6].
• Loss of Mixl1 function results in reduced recruitment of the definitive endoderm, and causes cells in the endoderm to remain stationary during gastrulation [5].
• Immunofluorescence and immunoelectron microscopy experiments with macrophage-like cells, Mm1, showed that ninein is localised specifically in the pericentriolar matrix of the centrosome [9].
• Approximately 30% of cell line cells Mm1 which lack la antigen, as well as of thioglycollate-induced peritoneal macrophages from SL/Am mice (TGC-M phi) could ingest unopsonized quail red cells (QRC) [8].

Associations of Mixl1 with chemical compounds

• A lectinlike receptor on murine macrophage cell line cells, Mm1: involvement of sialic acid-binding sites in opsonin-independent phagocytosis for xenogeneic red cells [8].
• Phagocytoses of tritiated thymidine-labeled bacteria by Mk1 and Mm1 were also enhanced when the bacteria had been opsonized with antibody [2].
• The antibody production of both 2,4,6-trinitrophenyl-keyhole limpet haemocyanin-primed splenocytes and B cell hybridomas was markedly reduced; about 20-40% of splenocytes and B cell hybridomas were killed by co-culture with IL-6-treated Mm1 [10].
• All precursor glycolipids and glycosyltransferases required to complete the biosynthetic pathway glucosylceramide (CMH) leads to lactosylceramide (CDH) leads to GA2 leads to gangliotetraosylceramide (GA1) leads to sialosylgangliotetraosylceramide (GM1b) were found in M1- and also in Mm1 cells [11].

Other interactions of Mixl1

• Mixl1-null ES cells, however, displayed a haematopoietic defect characterised by reduced and delayed Flk1 expression and a decrease in the frequency of haematopoietic CFCs [7].

Analytical, diagnostic and therapeutic context of Mixl1

• No requirement of divalent cation (Mg++, Ca++) and metabolic energy was observed for rosette formation between Mm1 cells and QRC [8].
• The flow cytometry pattern in IL-6-treated Mm1 was the same as that of cytochalasin B-treated Mm1 [12].
• The sensitivity of the target cells differed in co-cultures of antigen-primed splenocytes and B cell hybridomas with IL-6-treated Mm1 [10].

References