Erich E. Wanker

Flexible web-based integration of distributed large-scale human protein interaction maps (2007)

Chaurasia, Gautam, Iqbal, Yasir, Hänig, Christian, Herzel, Hanspeter, Wanker, Erich E., Futschik, Matthias E.

Protein-protein interactions constitute the backbone of many molecular processes. This has motivated the recent construction of several large-scale human protein-protein interaction maps [1-10]....

Plant nitric oxide synthase: a never-ending story? (2006)

Zemojtel, Tomasz, Fröhlich, Andreas, Palmieri, M. Cristina, Kolanczyk, Mateusz, Mikula, Ivan, Wyrwicz, Lucjan S., ...

Plant nitric oxide synthase: a never-ending story? (2006)

Zemojtel, Tomasz, Fröhlich, Andreas, Palmieri, M. Cristina, Kolanczyk, Mateusz, Mikula, Ivan, Wyrwicz, Lucjan S., ...

Plant nitric oxide synthase: a never-ending story? (2006)

Zemojtel, Tomasz, Fröhlich, Andreas, Palmieri, M. Cristina, Kolanczyk, Mateusz, Mikula, Ivan, Wyrwicz, Lucjan S., ...

Nuclear Oncoprotein Prothymosin {alpha} Is a Partner of Keap1: Implications for Expression of Oxidative Stress-Protecting Genes (2005)

Karapetian, Ruben N., Evstafieva, Alexandra G., Abaeva, Irina S., Chichkova, Nina V., Filonov, Grigoriy S., Rubtsov, Yuri P., ...

Animal cells counteract oxidative stress and electrophilic attack through coordinated expression of a set of detoxifying and antioxidant enzyme genes mediated by transcription factor Nrf2. In...

Method for qualitative comparisons of protein mixtures based on enzyme-catalyzed stable-isotope incorporation (2005)

Mirgorodskaya, Ekaterina, Wanker, Erich E., Otto, Albrecht, Lehrach, Hans, Gobom, Johan

Determining which proteins are unique among one or several protein populations is an often-encountered task in proteomics. To this purpose, we present a new method based on trypsin-catalyzed...

Generation of a yeast two-hybrid strain suitable for competitive protein binding analysis (2005)

Ralser, Markus, Goehler, Heike, Wanker, Erich E., Lehrach, Hans, Krobitsch, Sylvia

Ataxin-2 and huntingtin interact with endophilin-A complexes to function in plastin-associated pathways (2005)

Ralser, Markus, Nonhoff, Ute, Albrecht, Mario, Lengauer, Thomas, Wanker, Erich E., Lehrach, Hans, ...

Spinocerebellar ataxia type 2 is an inherited neurodegenerative disorder that is caused by an expanded trinucleotide repeat in the SCA2 gene, encoding a polyglutamine stretch in the gene product...

A human protein-protein interaction network : a resource for annotating the proteome (2005)

Stelzl, Ulrich, Worm, Uwe, Lalowski, Maciej, Haenig, Christian, Brembeck, Felix H., Goehler, Heike, ...

Protein-protein interaction maps provide a valuable framework for a better understanding of the functional organization of the proteome. To detect interacting pairs of human proteins systematically,...

A molecular pathogenesis for transcription factor associated poly-alanine tract expansions (2004)

Albrecht,Andrea N., Kornak,Uwe, Böddrich,Annett, Süring,Kathrin, Robinson,Peter N., Stiege,Asita C., ...

Poly-alanine (Ala) tract expansions in transcription factors have been shown to be associated with human birth defects such as malformations of the brain, the digits, and other structures. Expansions...

A protein interaction network links GIT1, an enhancer of huntingtin aggregation, to Huntington's Disease (2004)

Goehler,Heike, Lalowski,Maciej, Stelzl,Ulrich, Waelter,Stephanie, Stroedicke,Martin, Worm,Uwe, ...

Analysis of protein-protein interactions (PPIs) is a valuable approach for characterizing proteins of unknown function. Here, we have developed a strategy combining library and matrix yeast...

A molecular pathogenesis for transcription factor associated poly-alanine tract expansions (2004)

Albrecht, Andrea N., Kornak, Uwe, Böddrich, Annett, Süring, Kathrin, Robinson, Peter N., Stiege, Asita C., ...

Poly-alanine (Ala) tract expansions in transcription factors have been shown to be associated with human birth defects such as malformations of the brain, the digits, and other structures. Expansions...

A protein interaction network links GIT1, an enhancer of huntingtin aggregation, to Huntington's Disease (2004)

Goehler, Heike, Lalowski, Maciej, Stelzl, Ulrich, Waelter, Stephanie, Stroedicke, Martin, Worm, Uwe, ...

Analysis of protein-protein interactions (PPIs) is a valuable approach for characterizing proteins of unknown function. Here, we have developed a strategy combining library and matrix yeast...

Mutant huntingtin promotes the fibrillogenesis of wild-type huntingtin - A potential mechanism for loss of huntingtin function in Huntington's disease (2003)

Busch,Anne, Engemann,Sabine, Lurz,Rudi, Okazawa,Hitoshi, Lehrach,Hans, Wanker,Erich E.

Aggregation of huntingtin (htt) in neuronal inclusions is associated with the development of Huntington's disease (HD). Previously, we have shown that mutant htt fragments with polyglutamine (polyQ)...

Mutant huntingtin promotes the fibrillogenesis of wild-type huntingtin - A potential mechanism for loss of huntingtin function in Huntington's disease (2003)

Busch,Anne, Engemann,Sabine, Lurz,Rudi, Okazawa,Hitoshi, Lehrach,Hans, Wanker,Erich E.

Aggregation of huntingtin (htt) in neuronal inclusions is associated with the development of Huntington's disease (HD). Previously, we have shown that mutant htt fragments with polyglutamine (polyQ)...

Huntingtin fragments form aggresome-like inclusion bodies in mammalian cells (2003)

Boeddrich,Annett, Lurz,Rudi, Wanker,Erich E.

The formation of large perinuclear inclusion bodies containing protein aggregates was first described in HeLa cells. Woijcik et al. (1) have shown that treatment of HeLa cells with the proteasome...

Mutant huntingtin promotes the fibrillogenesis of wild-type huntingtin - A potential mechanism for loss of huntingtin function in Huntington's disease (2003)

Busch, Anne, Engemann, Sabine, Lurz, Rudi, Okazawa, Hitoshi, Lehrach, Hans, Wanker, Erich E.

Aggregation of huntingtin (htt) in neuronal inclusions is associated with the development of Huntington's disease (HD). Previously, we have shown that mutant htt fragments with polyglutamine (polyQ)...

Mutant huntingtin promotes the fibrillogenesis of wild-type huntingtin - A potential mechanism for loss of huntingtin function in Huntington's disease (2003)

Busch, Anne, Engemann, Sabine, Lurz, Rudi, Okazawa, Hitoshi, Lehrach, Hans, Wanker, Erich E.

Aggregation of huntingtin (htt) in neuronal inclusions is associated with the development of Huntington's disease (HD). Previously, we have shown that mutant htt fragments with polyglutamine (polyQ)...

Huntingtin fragments form aggresome-like inclusion bodies in mammalian cells (2003)

Boeddrich, Annett, Lurz, Rudi, Wanker, Erich E.

The formation of large perinuclear inclusion bodies containing protein aggregates was first described in HeLa cells. Woijcik et al. (1) have shown that treatment of HeLa cells with the proteasome...

Identification of benzothiazoles as potential polyglutamine aggregation inhibitors of Huntington's disease by using an automated filter retardation assay (2002)

Heiser,Volker, Engernann,Sabine, Brocker,Wolfgang, Dunkel,Ilona, Boeddrich,Annett, Waelter,Stefanie, ...

Preventing the formation of insoluble polyglutamine containing protein aggregates in neurons may represent an attractive therapeutic strategy to ameliorate Huntington's disease (HD). Therefore, the...

Identification of benzothiazoles as potential polyglutamine aggregation inhibitors of Huntington’s disease by using an automated filter retardation assay (2002)

Heiser,Volker, Engemann,Sabine, Bröcker,Wolfgang, Dunkel,Ilona, Boeddrich,Annett, Waelter,Stephanie, ...

Preventing the formation of insoluble polyglutamine containing protein aggregates in neurons may represent an attractive therapeutic strategy to ameliorate Huntington's disease (HD). Therefore, the...

Identification of benzothiazoles as potential polyglutamine aggregation inhibitors of Huntington's disease by using an automated filter retardation assay (2002)

Heiser,Volker, Engemann,Sabine, Bröcker,Wolfgang, Dunke,Ilona, Boeddrich,Annett, Waelter,Stephanie, ...

Preventing the formation of insoluble polyglutamine containing protein aggregates in neurons may represent an attractive therapeutic strategy to ameliorate Huntington's disease (HD). Therefore, the...

Aggregation of proteins with expanded glutamine and alanine repeats of the glutamine-rich and asparagine-rich domains of Sup35 and of the amyloid -peptide of amyloid plaques (2002)

Perutz,M. F., Pope,B. J., Owen,D., Wanker,Erich E., Scherzinger,E.

The exon-1 peptide of huntingtin has 51 Gln repeats and produces the symptoms of Huntington's disease in transgenic mice. Aggregation of the yeast Sup35 protein into prions has been attributed to its...

The synpolydactyly homolog (spdh) mutation in the mouse – a defect in patterning and growth of limb cartilage eleme (2002)

Albrecht,Andrea N., Schwabe,Georg C., Stricker,Sigmar, Böddrich,Annett, Wanker,Erich E., Mundlos,Stefan

We have investigated the recessive mouse mutant synpolydactyly homolog (spdh) as a model for human synpolydactyly (SPD). As in human SPD, the spdh phenotype consists of central polydactyly,...

The synpolydactyly homolog (spdh) mutation in the mouse – a defect in patterning and growth of limb cartilage eleme (2002)

Albrecht,Andrea N., Schwabe,Georg C., Stricker,Sigmar, Böddrich,Annett, Wanker,Erich E., Mundlos,Stefan

We have investigated the recessive mouse mutant synpolydactyly homolog (spdh) as a model for human synpolydactyly (SPD). As in human SPD, the spdh phenotype consists of central polydactyly,...

Identification of benzothiazoles as potential polyglutamine aggregation inhibitors of Huntington’s disease by using an automated filter retardation assay (2002)

Heiser, Volker, Engemann, Sabine, Bröcker, Wolfgang, Dunkel, Ilona, Boeddrich, Annett, Waelter, Stephanie, ...

Preventing the formation of insoluble polyglutamine containing protein aggregates in neurons may represent an attractive therapeutic strategy to ameliorate Huntington's disease (HD). Therefore, the...

The synpolydactyly homolog (spdh) mutation in the mouse – a defect in patterning and growth of limb cartilage eleme (2002)

Albrecht, Andrea N., Schwabe, Georg C., Stricker, Sigmar, Böddrich, Annett, Wanker, Erich E., Mundlos, Stefan

We have investigated the recessive mouse mutant synpolydactyly homolog (spdh) as a model for human synpolydactyly (SPD). As in human SPD, the spdh phenotype consists of central polydactyly,...

Hip1 and Hippi Participate in a Novel Cell Death-Signaling Pathway (2002)

Wanker, Erich E.

Neuronal apoptosis is a cardinal feature of late-onset neurodegenerative disorders such as Alzheimer's and Huntington's disease. Biochemical and cell biological studies point to a role for Hip1 and...

The synpolydactyly homolog (spdh) mutation in the mouse – a defect in patterning and growth of limb cartilage eleme (2002)

Albrecht, Andrea N., Schwabe, Georg C., Stricker, Sigmar, Böddrich, Annett, Wanker, Erich E., Mundlos, Stefan

We have investigated the recessive mouse mutant synpolydactyly homolog (spdh) as a model for human synpolydactyly (SPD). As in human SPD, the spdh phenotype consists of central polydactyly,...

Aggregation of proteins with expanded glutamine and alanine repeats of the glutamine-rich and asparagine-rich domains of Sup35 and of the amyloid -peptide of amyloid plaques (2002)

Perutz, M. F., Pope, B. J., Owen, D., Wanker, Erich E., Scherzinger, E.

The exon-1 peptide of huntingtin has 51 Gln repeats and produces the symptoms of Huntington's disease in transgenic mice. Aggregation of the yeast Sup35 protein into prions has been attributed to its...

Identification of benzothiazoles as potential polyglutamine aggregation inhibitors of Huntington's disease by using an automated filter retardation assay (2002)

Heiser, Volker, Engemann, Sabine, Bröcker, Wolfgang, Dunke, Ilona, Boeddrich, Annett, Waelter, Stephanie, ...

Preventing the formation of insoluble polyglutamine containing protein aggregates in neurons may represent an attractive therapeutic strategy to ameliorate Huntington's disease (HD). Therefore, the...

Identification of benzothiazoles as potential polyglutamine aggregation inhibitors of Huntington's disease by using an automated filter retardation assay (2002)

Heiser, Volker, Engernann, Sabine, Brocker, Wolfgang, Dunkel, Ilona, Boeddrich, Annett, Waelter, Stefanie, ...

Preventing the formation of insoluble polyglutamine containing protein aggregates in neurons may represent an attractive therapeutic strategy to ameliorate Huntington's disease (HD). Therefore, the...

Self-assembly of polyglutamine-containing huntingtin fragments into amyloid-like fibrils: Implications for Huntington’s disease pathology

Scherzinger, Eberhard, Sittler, Annie, Schweiger, Katja, Heiser, Volker, Lurz, Rudi, Hasenbank, Renate, ...

Huntington’s disease is a progressive neurodegenerative disorder caused by a polyglutamine [poly(Q)] repeat expansion in the first exon of the huntingtin protein. Previously, we showed that...

Hsp70 and Hsp40 chaperones can inhibit self-assembly of polyglutamine proteins into amyloid-like fibrils

Muchowski, Paul J., Schaffar, Gregor, Sittler, Annie, Wanker, Erich E., Hayer-Hartl, Manajit K., Hartl, F. Ulrich

The deposition of protein aggregates in neurons is a hallmark of neurodegenerative diseases caused by polyglutamine (polyQ) proteins. We analyzed the effects of the heat shock protein (Hsp) 70...

Inhibition of huntingtin fibrillogenesis by specific antibodies and small molecules: Implications for Huntington's disease therapy

Heiser, Volker, Scherzinger, Eberhard, Boeddrich, Annett, Nordhoff, Eckhard, Lurz, Rudi, Schugardt, Nancy, ...

The accumulation of insoluble protein aggregates in intra and perinuclear inclusions is a hallmark of Huntington's disease (HD) and related glutamine-repeat disorders. A central question is whether...

The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription

Steffan, Joan S., Kazantsev, Aleksey, Spasic-Boskovic, Olivera, Greenwald, Marilee, Zhu, Ya-Zhen, Gohler, Heike, ...

Huntington's Disease (HD) is caused by an expansion of a polyglutamine tract within the huntingtin (htt) protein. Pathogenesis in HD appears to include the cytoplasmic cleavage of htt and release of...

Huntingtin aggregation monitored by dynamic light scattering

Georgalis, Yannis, Starikov, E. B., Hollenbach, Birgit, Lurz, Rudi, Scherzinger, Eberhard, Saenger, Wolfram, ...

An initial stage of fibrillogenesis in solutions of glutathione S-transferase-huntingtin (GST-HD) fusion proteins has been studied by using dynamic light scattering. Two GST-HD systems with...

Accumulation of Mutant Huntingtin Fragments in Aggresome-like Inclusion Bodies as a Result of Insufficient Protein Degradation

Waelter, Stephanie, Boeddrich, Annett, Lurz, Rudi, Scherzinger, Eberhard, Lueder, Gerhild, Lehrach, Hans, ...

The huntingtin exon 1 proteins with a polyglutamine repeat in the pathological range (51 or 83 glutamines), but not with a polyglutamine tract in the normal range (20 glutamines), form aggresome-like...

Counting CAG repeats in the Huntington’s disease gene by restriction endonuclease EcoP15I cleavage

Möncke-Buchner, Elisabeth, Reich, Stefanie, Mücke, Merlind, Reuter, Monika, Messer, Walter, Wanker, Erich E., ...

Huntington’s disease (HD) is a progressive neurodegenerative disorder with autosomal-dominant inheritance. The disease is caused by a CAG trinucleotide repeat expansion located in the first exon of...

Identification of benzothiazoles as potential polyglutamine aggregation inhibitors of Huntington's disease by using an automated filter retardation assay

Heiser, Volker, Engemann, Sabine, Bröcker, Wolfgang, Dunkel, Ilona, Boeddrich, Annett, Waelter, Stephanie, ...

Preventing the formation of insoluble polyglutamine containing protein aggregates in neurons may represent an attractive therapeutic strategy to ameliorate Huntington's disease (HD). Therefore, the...

Polyglutamine fibrillogenesis: The pathway unfolds

Ross, Christopher A., Poirier, Michelle A., Wanker, Erich E., Amzel, Mario

Nuclear Oncoprotein Prothymosin α Is a Partner of Keap1: Implications for Expression of Oxidative Stress-Protecting Genes

Karapetian, Ruben N., Evstafieva, Alexandra G., Abaeva, Irina S., Chichkova, Nina V., Filonov, Grigoriy S., Rubtsov, Yuri P., ...

Animal cells counteract oxidative stress and electrophilic attack through coordinated expression of a set of detoxifying and antioxidant enzyme genes mediated by transcription factor Nrf2. In...

A potent small molecule inhibits polyglutamine aggregation in Huntington's disease neurons and suppresses neurodegeneration in vivo

Zhang, Xiaoqian, Smith, Donna L., Meriin, Anatoli B., Engemann, Sabine, Russel, Deborah E., Roark, Margo, ...

Polyglutamine (polyQ) disorders, including Huntington's disease (HD), are caused by expansion of polyQ-encoding repeats within otherwise unrelated gene products. In polyQ diseases, the pathology and...

Self-assembly of polyglutamine-containing huntingtin fragments into amyloid-like fibrils: Implications for Huntington’s disease pathology

Scherzinger, Eberhard, Sittler, Annie, Schweiger, Katja, Heiser, Volker, Lurz, Rudi, Hasenbank, Renate, ...

Huntington’s disease is a progressive neurodegenerative disorder caused by a polyglutamine [poly(Q)] repeat expansion in the first exon of the huntingtin protein. Previously, we showed that...

Hsp70 and Hsp40 chaperones can inhibit self-assembly of polyglutamine proteins into amyloid-like fibrils

Muchowski, Paul J., Schaffar, Gregor, Sittler, Annie, Wanker, Erich E., Hayer-Hartl, Manajit K., Hartl, F. Ulrich

The deposition of protein aggregates in neurons is a hallmark of neurodegenerative diseases caused by polyglutamine (polyQ) proteins. We analyzed the effects of the heat shock protein (Hsp) 70...

Inhibition of huntingtin fibrillogenesis by specific antibodies and small molecules: Implications for Huntington's disease therapy

Heiser, Volker, Scherzinger, Eberhard, Boeddrich, Annett, Nordhoff, Eckhard, Lurz, Rudi, Schugardt, Nancy, ...

The accumulation of insoluble protein aggregates in intra and perinuclear inclusions is a hallmark of Huntington's disease (HD) and related glutamine-repeat disorders. A central question is whether...

The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription

Steffan, Joan S., Kazantsev, Aleksey, Spasic-Boskovic, Olivera, Greenwald, Marilee, Zhu, Ya-Zhen, Gohler, Heike, ...

Huntington's Disease (HD) is caused by an expansion of a polyglutamine tract within the huntingtin (htt) protein. Pathogenesis in HD appears to include the cytoplasmic cleavage of htt and release of...

Huntingtin aggregation monitored by dynamic light scattering

Georgalis, Yannis, Starikov, E. B., Hollenbach, Birgit, Lurz, Rudi, Scherzinger, Eberhard, Saenger, Wolfram, ...

An initial stage of fibrillogenesis in solutions of glutathione S-transferase-huntingtin (GST-HD) fusion proteins has been studied by using dynamic light scattering. Two GST-HD systems with...

Accumulation of Mutant Huntingtin Fragments in Aggresome-like Inclusion Bodies as a Result of Insufficient Protein Degradation

Waelter, Stephanie, Boeddrich, Annett, Lurz, Rudi, Scherzinger, Eberhard, Lueder, Gerhild, Lehrach, Hans, ...

The huntingtin exon 1 proteins with a polyglutamine repeat in the pathological range (51 or 83 glutamines), but not with a polyglutamine tract in the normal range (20 glutamines), form aggresome-like...

Counting CAG repeats in the Huntington’s disease gene by restriction endonuclease EcoP15I cleavage

Möncke-Buchner, Elisabeth, Reich, Stefanie, Mücke, Merlind, Reuter, Monika, Messer, Walter, Wanker, Erich E., ...

Huntington’s disease (HD) is a progressive neurodegenerative disorder with autosomal-dominant inheritance. The disease is caused by a CAG trinucleotide repeat expansion located in the first exon of...

Identification of benzothiazoles as potential polyglutamine aggregation inhibitors of Huntington's disease by using an automated filter retardation assay

Heiser, Volker, Engemann, Sabine, Bröcker, Wolfgang, Dunkel, Ilona, Boeddrich, Annett, Waelter, Stephanie, ...

Preventing the formation of insoluble polyglutamine containing protein aggregates in neurons may represent an attractive therapeutic strategy to ameliorate Huntington's disease (HD). Therefore, the...

Polyglutamine fibrillogenesis: The pathway unfolds

Ross, Christopher A., Poirier, Michelle A., Wanker, Erich E., Amzel, Mario

Nuclear Oncoprotein Prothymosin α Is a Partner of Keap1: Implications for Expression of Oxidative Stress-Protecting Genes

Karapetian, Ruben N., Evstafieva, Alexandra G., Abaeva, Irina S., Chichkova, Nina V., Filonov, Grigoriy S., Rubtsov, Yuri P., ...

Animal cells counteract oxidative stress and electrophilic attack through coordinated expression of a set of detoxifying and antioxidant enzyme genes mediated by transcription factor Nrf2. In...

A potent small molecule inhibits polyglutamine aggregation in Huntington's disease neurons and suppresses neurodegeneration in vivo

Zhang, Xiaoqian, Smith, Donna L., Meriin, Anatoli B., Engemann, Sabine, Russel, Deborah E., Roark, Margo, ...

Polyglutamine (polyQ) disorders, including Huntington's disease (HD), are caused by expansion of polyQ-encoding repeats within otherwise unrelated gene products. In polyQ diseases, the pathology and...

UniHI: an entry gate to the human protein interactome

Chaurasia, Gautam, Iqbal, Yasir, Hänig, Christian, Herzel, Hanspeter, Wanker, Erich E., Futschik, Matthias E.

Systematic mapping of protein–protein interactions has become a central task of functional genomics. To map the human interactome, several strategies have recently been pursued. The generated...

An arginine/lysine-rich motif is crucial for VCP/p97-mediated modulation of ataxin-3 fibrillogenesis

Boeddrich, Annett, Gaumer, Sébastien, Haacke, Annette, Tzvetkov, Nikolay, Albrecht, Mario, Evert, Bernd O, ...

Arginine/lysine-rich motifs typically function as targeting signals for the translocation of proteins to the nucleus. Here, we demonstrate that such a motif consisting of four basic amino acids in...

Transcriptional repression induces a slowly progressive atypical neuronal death associated with changes of YAP isoforms and p73

Hoshino, Masataka, Qi, Mei-ling, Yoshimura, Natsue, Miyashita, Tomoyuki, Tagawa, Kazuhiko, Wada, Yo-ichi, ...

Transcriptional disturbance is implicated in the pathology of polyglutamine diseases, including Huntington's disease (HD). However, it is unknown whether transcriptional repression leads to neuronal...