C. von Eichel-Streiber

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UDP-glucose Deficiency Causes Hypersensitivity to the Cytotoxic Effect of Clostridium perfringens Phospholipase C*

S. Cole, M. Flores-Díaz, A. Alape-Girón, 1998, Journal of Biological Chemistry.

Large clostridial cytotoxins--a family of glycosyltransferases modifying small GTP-binding proteins.

P. Boquet, C. von Eichel-Streiber, M. Thelestam, 1996, Trends in microbiology.

Expression and prognostic relevance of annexin A3 in prostate cancer.

Martin Schostak, Helmut Klocker, Hartwig Huland, 2008, European urology.

Characterization of the cleavage site and function of resulting cleavage fragments after limited proteolysis of Clostridium difficile toxin B (TcdB) by host cells.

H. Urlaub, H. Söling, C. von Eichel-Streiber, 2005, Microbiology.

A comparative biochemical, pharmacological and immunological study of Clostridium novyi alpha-toxin, C. difficile toxin B and C. sordellii lethal toxin.

C. von Eichel-Streiber, A. Oksche, M. Popoff, 1991, Toxicon : official journal of the International Society on Toxinology.

Clostridium difficile IStron CdISt1: Discovery of a Variant Encoding Two Complete Transposase-Like Proteins

M. Moos, C. von Eichel-Streiber, C. Nitsche, 2004, Journal of bacteriology.

Purification of two high molecular weight toxins of Clostridium difficile which are antigenically related.

C. von Eichel-Streiber, U. Hadding, U. Harperath, 1987, Microbial pathogenesis.

Clostridium difficile toxin B acts on the GTP-binding protein Rho.

K. Aktories, P. Boquet, C. von Eichel-Streiber, 1994, The Journal of biological chemistry.

Transient expression of RhoA, -B, and -C GTPases in HeLa cells potentiates resistance to Clostridium difficile toxins A and B but not to Clostridium sordellii lethal toxin

P. Boquet, C. von Eichel-Streiber, M. Giry, 1995, Infection and immunity.

Induction of antitoxin responses in Clostridium-difficile-infected patients compared to healthy blood donors.

C. von Eichel-Streiber, Stuart Johnson, K. Knight, 2016, Anaerobe.

Glucosylation of small GTP-binding Rho proteins disrupts endothelial barrier function.

N. Suttorp, S. Hippenstiel, K. Aktories, 1997, The American journal of physiology.

UDP-Glucose Deficiency in a Mutant Cell Line Protects against Glucosyltransferase Toxins from Clostridium difficile and Clostridium sordellii(*)

E. Chaves-Olarte, P. Boquet, C. von Eichel-Streiber, 1996, The Journal of Biological Chemistry.

Inhibition of Receptor Signaling to Phospholipase D by Clostridium difficile Toxin B

K. Jakobs, C. von Eichel-Streiber, J. Keller, 1996, The Journal of Biological Chemistry.

Restoration of Clostridium difficile toxin-B-inhibited phospholipase D by phosphatidylinositol 4,5-bisphosphate.

K. Jakobs, C. von Eichel-Streiber, J. Keller, 1996, European journal of biochemistry.

Increased number of Clostridium difficile infections and prevalence of Clostridium difficile PCR ribotype 001 in southern Germany.

C. von Eichel-Streiber, J. Brazier, S. Borgmann, 2008, Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin.

Inhibition of small G proteins of the Rho family by statins or Clostridium difficile toxin B enhances cytokine‐mediated induction of NO synthase II

U. Förstermann, C. von Eichel-Streiber, F. Rodríguez-Pascual, 2000, British journal of pharmacology.

Variant toxin B and a functional toxin A produced by Clostridium difficile C34.

M. Moos, C. von Eichel-Streiber, M. Mehlig, 2001, FEMS microbiology letters.

Purification and evaluation of large clostridial cytotoxins that inhibit small GTPases of Rho and Ras subfamilies.

M. Moos, C. von Eichel-Streiber, 2000, Methods in enzymology.

The actin-based motility of intracellular Listeria monocytogenes is not controlled by small GTP-binding proteins of the Rho- and Ras-subfamilies.

J. Wehland, M. Rohde, T. Chakraborty, 1999, FEMS microbiology letters.

Small GTP-binding proteins of the Rho- and Ras-subfamilies are not involved in the actin rearrangements induced by attaching and effacing Escherichia coli.

M. Rohde, T. Chakraborty, C. von Eichel-Streiber, 1998, FEMS microbiology letters.

Genetic rearrangements in the pathogenicity locus of Clostridium difficile strain 8864 – implications for transcription, expression and enzymatic activity of toxins A and B

M. Weidmann, C. von Eichel-Streiber, P. Leukel, 1998, Molecular and General Genetics MGG.

Specific Inhibition of Phorbol Ester-stimulated Phospholipase D by Clostridium sordellii Lethal Toxin and Clostridium difficile Toxin B-1470 in HEK-293 Cells

K. Jakobs, J. de Gunzburg, C. von Eichel-Streiber, 1998, The Journal of Biological Chemistry.

Delineation of the catalytic domain of Clostridium difficile toxin B-10463 to an enzymatically active N-terminal 467 amino acid fragment.

M. Weidmann, M. Moos, C. von Eichel-Streiber, 1997, FEMS microbiology letters.

Transcription analysis of the genes tcdA-E of the pathogenicity locus of Clostridium difficile.

M. Weidmann, T. Hundsberger, C. von Eichel-Streiber, 1997, European journal of biochemistry.

Probing the action of Clostridium difficile toxin B in Xenopus laevis oocytes.

K. Aktories, C. von Eichel-Streiber, H. Richter, 1994, Journal of cell science.

Clostridium difficile toxins A and B inhibit human immune response in vitro

C. von Eichel-Streiber, U. Hadding, W. Däubener, 1988, Infection and immunity.

A Novel Toxinotyping Scheme and Correlation of Toxinotypes with Serogroups of Clostridium difficileIsolates

M. Delmée, C. von Eichel-Streiber, M. Rupnik, 1998, Journal of Clinical Microbiology.

Morphological changes of cultured endothelial cells after microinjection of toxins that act on the cytoskeleton

C. von Eichel-Streiber, E. Habermann, H. Müller, 1992, Infection and immunity.

Characterization of polymorphisms in the toxin A and B genes of Clostridium difficile.

C. von Eichel-Streiber, M. Rupnik, M. Hofstetter, 1997, FEMS microbiology letters.

Revised nomenclature of Clostridium difficile toxins and associated genes.

N. Fairweather, D. Gerding, B. Wren, 2005, Journal of medical microbiology.

Characterisation of cryptic plasmids in clinical isolates of Bacteroides fragilis.

C. von Eichel-Streiber, M. Dierich, D. Weinblum, 1985, Journal of medical microbiology.

Nucleotide sequence of Clostridium difficile toxin A.

C. von Eichel-Streiber, M. Sauerborn, 1990, Nucleic acids research.

Cloning and characterization of overlapping DNA fragments of the toxin A gene of clostridium difficile.

D. Suckau, C. von Eichel-Streiber, U. Hadding, 1989, Journal of general microbiology.

A nonsense mutation abrogates production of a functional enterotoxin A in Clostridium difficile toxinotype VIII strains of serogroups F and X.

C. von Eichel-Streiber, M. Rupnik, M. Grabnar, 1999, FEMS microbiology letters.

Inhibition of Fc epsilon-RI-mediated activation of rat basophilic leukemia cells by Clostridium difficile toxin B (monoglucosyltransferase)

K. Aktories, C. von Eichel-Streiber, I. Just, 1996, The Journal of biological chemistry.

Morphological changes in adherent cells induced by Clostridium difficile toxins.

C. von Eichel-Streiber, U. Hadding, M. Sauerborn, 1991, Biochemical Society transactions.

Oral Immunotherapy with Human Secretory IgA Improves Survival in the Hamster Model of Clostridioides difficile Infection.

C. von Eichel-Streiber, E. Chiari, M. Pulse, 2021, The Journal of infectious diseases.

Rac1 and PAK1 are upstream of IKK-epsilon and TBK-1 in the viral activation of interferon regulatory factor-3.

S. Pleschka, T. Wolff, C. Ehrhardt, 2004, FEBS letters.

The C-terminal ligand-binding domain of Clostridium difficile toxin A (TcdA) abrogates TcdA-specific binding to cells and prevents mouse lethality.

C. von Eichel-Streiber, M. Sauerborn, P. Leukel, 1997, FEMS microbiology letters.

Definition of the single integration site of the pathogenicity locus in Clostridium difficile.

T. Hundsberger, C. von Eichel-Streiber, M. Sauerborn, 1996, Gene.

Evidence for a modular structure of the homologous repetitive C-terminal carbohydrate-binding sites of Clostridium difficile toxins and Streptococcus mutans glucosyltransferases

H. Kuramitsu, C. von Eichel-Streiber, M. Sauerborn, 1992, Journal of bacteriology.

GTPases of the Rho Subfamily Are Required for Brucella abortus Internalization in Nonprofessional Phagocytes

C. Guzmán-Verri, E. Chaves-Olarte, S. Arvidson, 2001, The Journal of Biological Chemistry.

Clostridium difficile Toxins Disrupt Epithelial Barrier Function by Altering Membrane Microdomain Localization of Tight Junction Proteins

P. Verkade, C. Parkos, J. Madara, 2001, Infection and Immunity.

Ras, Rap, and Rac Small GTP-binding Proteins Are Targets for Clostridium sordellii Lethal Toxin Glucosylation (*)

D. Cussac, B. Antonny, P. Chavrier, 1996, The Journal of Biological Chemistry.

Rac1 and PAK1 are upstream of IKK‐ε and TBK‐1 in the viral activation of interferon regulatory factor‐3

S. Pleschka, T. Wolff, C. Ehrhardt, 2004 .

Impact of amino acids 22-27 of Rho-subfamily GTPases on glucosylation by the large clostridial cytotoxins TcsL-1522, TcdB-1470 and TcdB-8864.

S. Müller, M. Moos, C. von Eichel-Streiber, 1999, European journal of biochemistry.

Cellular UDP-Glucose Deficiency Caused by a Single Point Mutation in the UDP-Glucose Pyrophosphorylase Gene*

B. Persson, M. Flores-Díaz, A. Alape-Girón, 1997, The Journal of Biological Chemistry.

The Enterotoxin from Clostridium difficile (ToxA) Monoglucosylates the Rho Proteins(*)

M. Wilm, K. Aktories, C. von Eichel-Streiber, 1995, The Journal of Biological Chemistry.

Activation of NF‐κB and IL‐8 by Yersinia enterocolitica invasin protein is conferred by engagement of Rac1 and MAP kinase cascades

M. Aepfelbacher, M. Kracht, I. Autenrieth, 2003, Cellular microbiology.

Control of cellular phosphatidylinositol 4,5-bisphosphate levels by adhesion signals and rho GTPases in NIH 3T3 fibroblasts involvement of both phosphatidylinositol-4-phosphate 5-kinase and phospholipase C.

Chunyi Zhang, K. Jakobs, C. Zhang, 2000, European journal of biochemistry.

Clostridium difficile toxin A carries a C-terminal repetitive structure homologous to the carbohydrate binding region of streptococcal glycosyltransferases.

C. von Eichel-Streiber, M. Sauerborn, C. Eichel-Streiber, 1990, Gene.

Rho protein inhibition blocks protein kinase C translocation and activation.

N. Suttorp, S. Hippenstiel, C. von Eichel-Streiber, 1998, Biochemical and biophysical research communications.

Activation of astroglial phospholipase D activity by phorbol ester involves ARF and Rho proteins.

J. B. Park, S. Ryu, C. von Eichel-Streiber, 2000, Biochimica et biophysica acta.

Four distinct structural domains in Clostridium difficile toxin B visualized using SAXS.

N. Fairweather, D. Svergun, E. Carpenter, 2010, Journal of molecular biology.

Demonstration that the Group II Intron from the Clostridial Conjugative Transposon Tn5397 Undergoes Splicing In Vivo

A. Roberts, C. von Eichel-Streiber, P. Mullany, 2001, Journal of bacteriology.

A chimeric ribozyme in Clostridium difficile combines features of group I introns and insertion elements

M. Moos, C. von Eichel-Streiber, M. Rupnik, 2000, Molecular microbiology.

Inhibition of FcRI-mediated Activation of Rat Basophilic Leukemia Cells by Clostridium difficile Toxin B (Monoglucosyltransferase) (*)

K. Aktories, C. von Eichel-Streiber, I. Just, 1996, The Journal of Biological Chemistry.

The low molecular mass GTP-binding protein Rho is affected by toxin A from Clostridium difficile.

K. Aktories, C. von Eichel-Streiber, I. Just, 1995, The Journal of clinical investigation.

The IStron CdISt1 of Clostridium difficile: molecular symbiosis of a group I intron and an insertion element.

C. von Eichel-Streiber, C. Nitsche, O. Hasselmayer, 2004, Anaerobe.

Treatment and Prevention of Recurrent Clostridium difficile Infection with Functionalized Bovine Antibody-Enriched Whey in a Hamster Primary Infection Model

U. Kulozik, H. Kliem, M. Pfaffl, 2019, Toxins.

Regulation of phospholipase D activity in synaptosomes permeabilized with Staphylococcus aureus α‐toxin

O. Weichel, C. von Eichel-Streiber, A. Valeva, 1998 .

A Novel Cytotoxin from Clostridium difficileSerogroup F Is a Functional Hybrid between Two Other Large Clostridial Cytotoxins*

M. Weidmann, E. Chaves-Olarte, C. von Eichel-Streiber, 1999, The Journal of Biological Chemistry.