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M Birke

Publications and source records attributed to M Birke.

7 recordsLinked to original sources
PubMed2003

Observation of the conduction electron spin polarization in the Ag spacer of a Fe/Fg/Fe trilayer.

The spatially oscillating electron spin polarization in the Ag spacer of a 4 nm Fe/20 nmAg/4 nm Fe(001) epitaxial trilayer has been determined by means of low energy muon spin rotation. It oscillates with the same period as the interlayer exchange coupling, but shows a much weaker attenuation at large distances x from the interface. The measured magnetization profile from the inner 14 nm of the spacer is described by an oscillating polarization decaying as x(-0.8(1)). This unusual behavior may arise from a full confinement of electron states within the spacer.

Journal Article↗
PubMed2001

MLL-ENL causes a reversible and myc-dependent block of myelomonocytic cell differentiation.

The translocation t(11;19) is a recurrent feature of a subgroup of acute leukemias occurring in infants. This event fuses the genes MLL and ENL and creates the leukemogenic oncoprotein MLL-ENL. We studied the effect of retroviral MLL-ENL expression in primary mouse hematopoietic cells and show here that MLL-ENL requires the oncoprotein Myc to establish a reversible differentiation arrest of a myelomonocytic precursor population. MLL-ENL-transduced cells proliferated as immature myeloid cells in the presence of interleukin 3. The addition of granulocyte colony-stimulating factor reversed the maturation block set by MLL-ENL and induced the development of mature granulocytes and macrophages accompanied by growth arrest. Gene expression analysis indicated a down-regulation of the proto-oncogene c-myc and of several c-myc target genes during granulocyte colony-stimulating factor-mediated differentiation. The role of c-myc in the MLL-ENL transformation pathway was tested by modulating the effective Myc protein concentrations in MLL-ENL transduced cells. Cotransduction of dominant-negative Myc neutralized the MLL-ENL effect and precluded transformation. In contrast, constitutive expression of Myc cooperated with MLL-ENL and caused the transformation of a cell population with an irreversible maturation arrest.

Animals↗
PubMed2001

The ENL moiety of the childhood leukemia-associated MLL-ENL oncoprotein recruits human Polycomb 3.

The translocation t(11;19) is frequently found in acute leukemia in infants. This event truncates the proto-oncogene MLL and fuses the 5' end of MLL in frame with the ENL gene. ENL contributes a crucial protein-protein interaction domain to the resulting oncoprotein MLL-ENL. Here we show by yeast two-hybrid assays, GST-pull-down experiments and in a far western blot analysis that this domain is necessary and sufficient to recruit a novel member of the human Polycomb protein family (hPc3). hPc3 RNA was detected throughout the human hematopoietic system. Similar to other Polycomb proteins hPc3 acts as a transcriptional repressor. The ENL-hPc3 interaction was verified by mutual co-precipitation of the proteins from cell extracts. ENL and hPc3 tagged with fluorescent proteins co-localized in living cells in a nuclear dot pattern. An internal region of hPc3 was responsible for binding to ENL. Finally, hPc3 binds to the C-terminus of AF9, another common MLL fusion partner. The recruitment of a repressive function by ENL opens up a new insight into a possible mechanism of leukemogenesis by the fusion protein MLL-ENL.

Amino Acid Sequence↗
PubMed2000

ENL, the MLL fusion partner in t(11;19), binds to the c-Abl interactor protein 1 (ABI1) that is fused to MLL in t(10;11)+.

Translocations of the chromosomal locus 11q23 that disrupt the MLL gene (alternatively ALL-1 or HRX) are frequently found in children's leukemias. These events fuse the MLL amino terminus in frame with a variety of unrelated proteins. Up to date, 16 different fusion partners have been characterized and more are likely to exist. No general unifying property could yet be detected amongst these proteins. We show here that the frequent MLL fusion partner ENL at 19p13.1 interacts with the human homologue of the mouse Abl-Interactor 1 (ABI1) protein. ABI1 in turn, is fused to MLL in the t(10;11)(p11.2;q23) translocation. ABI1 was identified as an ENL binding protein by a yeast two-hybrid screen. The interaction of ENL and ABI1 could be verified in vitro by far-Western blot assays and GST-pulldown studies as well as in vivo by co-immunoprecipitation experiments. A structure-function analysis identified an internal region of ENL and a composite motif of ABI1 including an SH3 domain as mutual binding partners. These data introduce novel aspects that might contribute to the understanding of the process of leukemogenesis by MLL fusion proteins.

Adaptor Proteins, Signal Transducing↗
PubMed1977

Visual following in newborns: role of figure-ground contrast and configurational detail.

Visual pursuit was used in studying the ability of newborn infants to discriminate levels of contrast. Ratings of the degree of eye and head following were made as subjects pursued facial targets which varied in terms of the degree fo figure-gound contrast and te degree of contrast internal to the figure as defined by the presence of contrast such that the strongest pursuit occurred to stimuli which had clearly discriminable facial detailing in addition to strong figure-ground contrast. These results suggest that the newborn is sensitive not only to large border areas of high contrasting illumination but to finer configurational details of stimuli as well.

Attention↗