Disease relevance of Bcl11a

• Evi9 is a common site of retroviral integration in BXH2 murine myeloid leukemias [1].
• Differentiation inhibitory factor (nm23 protein) inhibited the induction of differentiation of mouse myeloid leukemia M1 and WEHI-3BD+ and human erythroleukemia HEL, KU812, and K562 cells [2].
• Characteristics of the karyotypes of the mouse myeloid leukemia in comparison with other leukemias were noted [3].

High impact information on Bcl11a

• A 3.7 kb mRNA coding for the G-CSF receptor could be detected in mouse myeloid leukemia NFS-60 and WEHI-3B D+ cells as well as in bone marrow cells [4].
• Two cDNAs encoding the receptor for murine granulocyte colony-stimulating factor (G-CSF) were isolated from a CDM8 expression library of mouse myeloid leukemia NFS-60 cells, and their nucleotide sequences were determined [4].
• Mice transplanted with Bcl11a-deficient cells died from T cell leukemia derived from the host [5].
• Here we show that Bcl11a is essential for postnatal development and normal lymphopoiesis [5].
• The gene Bcl11b, which encodes zinc finger proteins, and its paralog, Bcl11a, are associated with immune-system malignancies [6].

Biological context of Bcl11a

• Thus, Bcl11a may also function as a non-autonomous T cell tumor suppressor gene [5].
• Bcl11a (also called Evi9) functions as a myeloid or B cell proto-oncogene in mice and humans, respectively [5].
• Human EVI9, located on the chromosome 2p13 region, contains an open reading frame of 797 amino acids that is 98.7% identical to the mouse protein [7].
• Here, we describe the expression patterns of CTIP1 and CTIP2 during mouse embryogenesis and in the post-natal brain [8].
• The homeobox gene Hox-2.4 is transcriptionally activated in cells of the mouse myeloid leukemia WEHI-3B [9].

Anatomical context of Bcl11a

• Evi9a and Evi9c, but not Evi9b, show transforming activity for NIH 3T3 cells, suggesting that Evi9 is a dominantly acting proto-oncogene [1].
• Human EVI9, a homologue of the mouse myeloid leukemia gene, is expressed in the hematopoietic progenitors and down-regulated during myeloid differentiation of HL60 cells [7].
• Differentiation of a cell line of mouse myeloid leukemia. I. Simultaneous induction of lysosomal enzyme activities and phagocytosis [10].
• Mouse myeloid leukemia (Ml) cells both in vitro and in vivo can be induced to differentiate into macrophages and granulocytes by various compounds [11].
• A factor inducing differentiation of mouse myeloid leukemia cells in human amniotic fluid [12].

Associations of Bcl11a with chemical compounds

• The protein and DNA contents of mouse myeloid leukemia M1 (clone B24) cells were determined by flow cytometry (FCM) after double fluorescent staining of the cells with fluorescein isothiocyanate and propidium iodide [13].
• The methanol extract of the aerial part of Andrographis paniculata Nees showed potent cell differentiation-inducing activity on mouse myeloid leukemia (M1) cells [14].
• Six pregnane glycosides and three cardenolides were isolated as differentiation inducers using mouse myeloid leukemia (Ml) cells from Periplocae Radicis Cortex (bark of Periploca sepium BGE., Asclepiadaceae) [15].
• The effect of DL-alpha-tocopherol on the differentiation of the mouse myeloid leukemia cell line (M1) was investigated using fluorometry [16].
• M1 cells derived from mouse myeloid leukemia have been reported to differentiate to macrophage-like cells upon treatment with substances such as lipopolysaccharide [17].

Other interactions of Bcl11a

• The expression status of mitochondrial uncoupling protein 2 (UCP2) was investigated in undifferentiated mouse myeloid leukemia (M1) and its differentiated macrophage-like cells (Mm1) [18].

Analytical, diagnostic and therapeutic context of Bcl11a

• Transplantation studies show that these defects in Bcl11a mutant mice are intrinsic to fetal liver precursor cells [5].

References