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M Busslinger

Publications and source records attributed to M Busslinger.

95 records · Page 6Linked to original sources

Regulation of human epsilon germline transcription: role of B-cell-specific activator protein.

Germline transcripts initiate from promoters upstream of the immunoglobulin switch region, and are necessary to target the appropriate switch region for recombination and switching. Different cytokines activate transcription at the appropriate germline promoter. Because binding sites for B-cell-specific activator protein (BSAP) are located upstream of several switch regions in the immunoglobulin heavy chain gene cluster, BSAP might play a role in the regulation of germline transcription and isotype switching. We investigated whether BSAP plays a role in the transcriptional regulation of the epsilon germline promoter in human B cells. Our results showed that BSAP plays a role in both IL-4-dependent induction and CD40-mediated upregulation of human epsilon germline transcription. BSAP is unique among the transcription factors that regulate epsilon germline expression, because it is B cell specific, and is at the merging point of two signalling pathways that are critical for IgE switching.

B-Lymphocytes↗

Normal brainstem auditory evoked potentials in Pax5-deficient mice despite morphologic alterations in the auditory midbrain region.

The inferior colliculus in the auditory midbrain region is underdeveloped near the midline in mice lacking the transcription factor Pax5. We have now tested whether hearing deficiencies occur in these mice by measuring auditory evoked brainstem responses. However, the responses and audiograms obtained in homozygous Pax5 mutants did not differ from those of control mice, suggesting that the observed morphologic alterations of the inferior colliculus do not affect hearing, as judged by auditory evoked potential recordings. The only detectable effect of the Pax5 mutation was a delay in the development of the auditory sensitivity and response latency that correlates with the general growth retardation observed in these mice.

Age Factors↗