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Michael Bachmann

Researcher at Helmholtz-Zentrum Dresden-Rossendorf

Publications -  402
Citations -  16252

Michael Bachmann is an academic researcher from Helmholtz-Zentrum Dresden-Rossendorf. The author has contributed to research in topics: Antigen & Chimeric antigen receptor. The author has an hindex of 63, co-authored 360 publications receiving 14388 citations. Previous affiliations of Michael Bachmann include ACADIA Pharmaceuticals Inc. & University of Southern California.

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Journal ArticleDOI

The La antigen shuttles between the nucleus and the cytoplasm in CV-1 cells.

TL;DR: The antibody gives a nuclear speckled type staining and a perinuclear cytoplasmic staining on cultured cells in immunofluorescence microscopy and the transport into the nucleus apparently depends on glycosylation.
Journal ArticleDOI

Characterization of the autoantigen La (SS-B) as a dsRNA unwinding enzyme

TL;DR: In this article, an ATP-dependent double-stranded RNA unwinding activity was detected, which could be inhibited by monospecific anti-La antibodies, and the La protein was able to melt dsRNA substrates with either two 3'-overhangs or a single 3'-and a 5'-overhang.
Book ChapterDOI

Native polyacrylamide gels.

TL;DR: A starting protocol for "native" PAGE, where the charge of each of the proteins will depend on the primary amino acid sequence of the protein (isoelectric point) and the pH during electrophoresis, will mainly influence the mobility of the respective protein during electophoresis.
Journal ArticleDOI

Shuttling of the autoantigen La between nucleus and cell surface after uv irradiation of human keratinocytes.

TL;DR: It is established that the nuclear autoantigen La shuttles between the nucleus and the cytoplasm in tumor cells after inhibition of transcription or virus infection, and primary human keratinocytes from both healthy donors and patients with xeroderma pigmentosum were reinvestigated.
Journal ArticleDOI

Nucleic acid template and the risk of a PCR-Induced HIV-1 drug resistance mutation.

TL;DR: UDPS on clones and site-directed mutants containing subtype B- and C-specific patterns of silent mutations in the conserved KKK motif encompassing RT codons 64 to 66 found that subtype-specific nucleotide differences were responsible for increased PCR-induced K65R mutation in subtype C viruses.