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825 results on '"Sakmar, Thomas P."'

4. Autoantibodies targeting G protein-coupled receptors: An evolving history in autoimmunity. Report of the 4th international symposium

Author

Cabral-Marques, Otávio, Moll, Guido, Catar, Rusan, Preuß, Beate, Bankamp, Lukas, Pecher, Ann-Christin, Henes, Joerg, Klein, Reinhild, Kamalanathan, A.S., Akbarzadeh, Reza, van Oostveen, Wieke, Hohberger, Bettina, Endres, Matthias, Koolmoes, Bryan, Levarht, Nivine, Postma, Rudmer, van Duinen, Vincent, van Zonneveld, Anton Jan, de Vries-Bouwstra, Jeska, Fehres, Cynthia, Tran, Florian, do Vale, Fernando Yuri Nery, da Silva Souza, Kamilla Batista, Filgueiras, Igor Salerno, Schimke, Lena F., Baiocchi, Gabriela Crispim, de Miranda, Gustavo Cabral, da Fonseca, Dennyson Leandro Mathias, Freire, Paula Paccielli, Hackel, Alexander M., Grasshoff, Hanna, Stähle, Anja, Müller, Antje, Dechend, Ralf, Yu, Xinhua, Petersen, Frank, Sotzny, Franziska, Sakmar, Thomas P., Ochs, Hans D., Schulze-Forster, Kai, Heidecke, Harald, Scheibenbogen, Carmen, Shoenfeld, Yehuda, and Riemekasten, Gabriela

Published
2023
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5. The role of signaling pathways mediated by the GPCRs CysLTR1/2 in melanocyte proliferation and senescence.

Author

Huber, Thomas, Horioka-Duplix, Mizuho, Chen, Yuanhuang, Saca, Victoria R., Ceraudo, Emilie, Chen, Yu, and Sakmar, Thomas P.

Subjects
CELLULAR aging, MELANOMA, CELL growth, CELLULAR signal transduction, MELANOCYTES, G protein coupled receptors
Abstract

In contrast with sun exposure–induced melanoma, rarer melanocytic tumors and neoplasms with low mutational burden present opportunities to study isolated signaling mechanisms. These include uveal melanoma and blue nevi, which are often driven by mutations within the G protein–coupled signaling cascade downstream of cysteinyl leukotriene receptor 2. Here, we review how the same mutations within this pathway drive the growth of melanocytes in one tissue but can inhibit the growth of those in another, exemplifying the role of the tissue environment in the delicate balance between uncontrolled cell growth and senescence. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Multiplexed mapping of the interactome of GPCRs with receptor activity-modifying proteins

Author

Kotliar, Ilana B., Bendes, Annika, Dahl, Leo, Chen, Yuanhuang, Saarinen, Marcus, Ceraudo, Emilie, Dodig-Crnkovic, Tea, Uhlén, Mathias, Svenningsson, Per, Schwenk, Jochen M., Sakmar, Thomas P., Kotliar, Ilana B., Bendes, Annika, Dahl, Leo, Chen, Yuanhuang, Saarinen, Marcus, Ceraudo, Emilie, Dodig-Crnkovic, Tea, Uhlén, Mathias, Svenningsson, Per, Schwenk, Jochen M., and Sakmar, Thomas P.

Abstract

Receptor activity-modifying proteins (RAMPs) form complexes with G protein-coupled receptors (GPCRs) and may regulate their cellular trafficking and pharmacology. RAMP interactions have been identified for about 50 GPCRs, but only a few GPCR-RAMP complexes have been studied in detail. To elucidate a comprehensive GPCR-RAMP interactome, we created a library of 215 dual epitope-tagged (DuET) GPCRs representing all GPCR subfamilies and coexpressed each GPCR with each of the three RAMPs. Screening the GPCR-RAMP pairs with customized multiplexed suspension bead array (SBA) immunoassays, we identified 122 GPCRs that showed strong evidence for interaction with at least one RAMP. We screened for interactions in three cell lines and found 23 endogenously expressed GPCRs that formed complexes with RAMPs. Mapping the GPCR-RAMP interactome expands the current system-wide functional characterization of RAMP-interacting GPCRs to inform the design of selective therapeutics targeting GPCR-RAMP complexes., QC 20240820

Published
2024
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8. Defeating Alzheimer's disease and other dementias: a priority for European science and society

Author

Winblad, Bengt, Amouyel, Philippe, Andrieu, Sandrine, Ballard, Clive, Brayne, Carol, Brodaty, Henry, Cedazo-Minguez, Angel, Dubois, Bruno, Edvardsson, David, Feldman, Howard, Fratiglioni, Laura, Frisoni, Giovanni B, Gauthier, Serge, Georges, Jean, Graff, Caroline, Iqbal, Khalid, Jessen, Frank, Johansson, Gunilla, Jönsson, Linus, Kivipelto, Miia, Knapp, Martin, Mangialasche, Francesca, Melis, René, Nordberg, Agneta, Rikkert, Marcel Olde, Qiu, Chengxuan, Sakmar, Thomas P, Scheltens, Philip, Schneider, Lon S, Sperling, Reisa, Tjernberg, Lars O, Waldemar, Gunhild, Wimo, Anders, and Zetterberg, Henrik

Subjects
Alzheimer Disease, Biomedical Research, Dementia, Europe, Humans, Clinical Sciences, Neurosciences, Neurology & Neurosurgery
Published
2016

24. Multiplexed selectivity screening of anti-GPCR antibodies

Author

Dahl, Leo, primary, Kotliar, Ilana B., additional, Bendes, Annika, additional, Dodig-Crnković, Tea, additional, Fromm, Samuel, additional, Elofsson, Arne, additional, Uhlén, Mathias, additional, Sakmar, Thomas P., additional, and Schwenk, Jochen M., additional

Published
2023
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26. Supplementary Tables S1-S11 from Combined Inhibition of Gαq and MEK Enhances Therapeutic Efficacy in Uveal Melanoma

Author

Hitchman, Tyler D., primary, Bayshtok, Gabriella, primary, Ceraudo, Emilie, primary, Moore, Amanda R., primary, Lee, Cindy, primary, Jia, Ruobing, primary, Wang, Naitao, primary, Pachai, Mohini R., primary, Shoushtari, Alexander N., primary, Francis, Jasmine H., primary, Guan, Youxin, primary, Chen, Juliet, primary, Chang, Matthew T., primary, Taylor, Barry S., primary, Sakmar, Thomas P., primary, Huber, Thomas, primary, Chi, Ping, primary, and Chen, Yu, primary

Published
2023
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27. Supplementary Figure S7 from Combined Inhibition of Gαq and MEK Enhances Therapeutic Efficacy in Uveal Melanoma

Author

Hitchman, Tyler D., primary, Bayshtok, Gabriella, primary, Ceraudo, Emilie, primary, Moore, Amanda R., primary, Lee, Cindy, primary, Jia, Ruobing, primary, Wang, Naitao, primary, Pachai, Mohini R., primary, Shoushtari, Alexander N., primary, Francis, Jasmine H., primary, Guan, Youxin, primary, Chen, Juliet, primary, Chang, Matthew T., primary, Taylor, Barry S., primary, Sakmar, Thomas P., primary, Huber, Thomas, primary, Chi, Ping, primary, and Chen, Yu, primary

Published
2023
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28. Supplementary Figures S1-S6 from Combined Inhibition of Gαq and MEK Enhances Therapeutic Efficacy in Uveal Melanoma

Author

Hitchman, Tyler D., primary, Bayshtok, Gabriella, primary, Ceraudo, Emilie, primary, Moore, Amanda R., primary, Lee, Cindy, primary, Jia, Ruobing, primary, Wang, Naitao, primary, Pachai, Mohini R., primary, Shoushtari, Alexander N., primary, Francis, Jasmine H., primary, Guan, Youxin, primary, Chen, Juliet, primary, Chang, Matthew T., primary, Taylor, Barry S., primary, Sakmar, Thomas P., primary, Huber, Thomas, primary, Chi, Ping, primary, and Chen, Yu, primary

Published
2023
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29. Multiplexed selectivity screening of anti-GPCR antibodies

Author

Dahl, Leo, Kotliar, Ilana B., Bendes, Annika, Dodig-Crnkovic, Tea, Fromm, Samuel, Elofsson, Arne, Uhlen, Mathias, Sakmar, Thomas P., Schwenk, Jochen M., Dahl, Leo, Kotliar, Ilana B., Bendes, Annika, Dodig-Crnkovic, Tea, Fromm, Samuel, Elofsson, Arne, Uhlen, Mathias, Sakmar, Thomas P., and Schwenk, Jochen M.

Abstract

G protein-coupled receptors (GPCRs) control critical cellular signaling pathways. Therapeutic agents including anti-GPCR antibodies (Abs) are being developed to modulate GPCR function. However, validating the selectivity of anti-GPCR Abs is challenging because of sequence similarities among individual receptors within GPCR sub-families. To address this challenge, we developed a multiplexed immunoassay to test >400 anti-GPCR Abs from the Human Protein Atlas targeting a customized library of 215 expressed and solubilized GPCRs representing all GPCR subfamilies. We found that-61% of Abs tested were selective for their intended target,-11% bound off -target, and-28% did not bind to any GPCR. Antigens of on-target Abs were, on average, significantly longer, more disordered, and less likely to be buried in the interior of the GPCR protein than the other Abs. These results provide important insights into the immunogenicity of GPCR epitopes and form a basis for designing therapeu-tic Abs and for detecting pathological auto-Abs against GPCRs.

Published
2023
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30. Elucidating the Interactome of G Protein-Coupled Receptors and Receptor Activity-Modifying Proteins

Author

Kotliar, Ilana B., Lorenzen, Emily, Schwenk, Jochen M., Hay, Debbie L., Sakmar, Thomas P., Kotliar, Ilana B., Lorenzen, Emily, Schwenk, Jochen M., Hay, Debbie L., and Sakmar, Thomas P.

Abstract

G protein-coupled receptors (GPCRs) are known to interact with several other classes of integral membrane proteins that modulate their biology and pharmacology. However, the extent of these interactions and the mechanisms of their effects are not well understood. For example, one class of GPCR-interacting proteins, receptor activity-modifying proteins (RAMPs), comprise three related and ubiquitously expressed single-transmembrane span proteins. The RAMP family was discovered more than two decades ago, and since then GPCR-RAMP interactions and their functional consequences on receptor trafficking and ligand selectivity have been documented for several secretin (class B) GPCRs, most notably the calcitonin receptor-like receptor. Recent bioinformatics and multiplexed experimental studies suggest that GPCR-RAMP interactions might bemuchmore widespread than previously anticipated. Recently, cryo-electron microscopy has provided high-resolution structures of GPCR-RAMP-ligand complexes, and drugs have been developed that target GPCR-RAMP complexes. In this review, we provide a summary of recent advances in techniques that allow the discovery of GPCR-RAMP interactions and their functional consequences and highlight prospects for future advances. We also provide an up-to-date list of reported GPCR-RAMP interactions based on a review of the current literature., QC 20230505

Published
2023
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37. Human Islet Amyloid Polypeptide (hIAPP) Protofibril‐Specific Antibodies for Detection and Treatment of Type 2 Diabetes (Adv. Sci. 34/2022)

Author

Bortoletto, Angelina S., primary, Graham, W. Vallen, additional, Trout, Gabriella, additional, Bonito‐Oliva, Alessandra, additional, Kazmi, Manija A., additional, Gong, Jing, additional, Weyburne, Emily, additional, Houser, Brandy L., additional, Sakmar, Thomas P., additional, and Parchem, Ronald J., additional

Published
2022
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38. Multiplexed selectivity screening of anti-GPCR antibodies

Author

Dahl, Leo, primary, Kotliar, Ilana B., additional, Bendes, Annika, additional, Dodig-Crnković, Tea, additional, Fromm, Samuel, additional, Elofsson, Arne, additional, Uhlén, Mathias, additional, Sakmar, Thomas P., additional, and Schwenk, Jochen M., additional

Published
2022
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41. Targeting of the pulmonary capillary vascular niche promotes lung alveolar repair and ameliorates fibrosis

Author

Cao, Zhongwei, Lis, Raphael, Ginsberg, Michael, Chavez, Deebly, Shido, Koji, Rabbany, Sina Y., Fong, Guo-Hua, Sakmar, Thomas P., Rafii, Shahin, and Ding, Bi-Sen

Subjects
Fibrosis -- Physiological aspects, Lung diseases -- Physiological aspects, Regeneration (Biology) -- Physiological aspects, Biological sciences, Health
Abstract

Although the lung can undergo self-repair after injury, fibrosis in chronically injured or diseased lungs can occur at the expense of regeneration. Here we study how a hematopoietic-vascular niche regulates alveolar repair and lung fibrosis. Using intratracheal injection of bleomycin or hydrochloric acid in mice, we show that repetitive lung injury activates pulmonary capillary endothelial cells (PCECs) and perivascular macrophages, impeding alveolar repair and promoting fibrosis. Whereas the chemokine receptor CXCR7, expressed on PCECs, acts to prevent epithelial damage and ameliorate fibrosis after a single round of treatment with bleomycin or hydrochloric acid, repeated injury leads to suppression of CXCR7 expression and recruitment of vascular endothelial growth factor receptor 1 (VEGFR1)-expressing perivascular macrophages. This recruitment stimulates Wnt/p-catenin-dependent persistentupregulation of the Notch ligand Jagged1 (encoded by Jag1) in PCECs, which in turn stimulates exuberant Notch signaling in perivascular fibroblasts and enhances fibrosis. Administration of a CXCR7 agonist or PCEC-targeted Jag1 shRNA after lung injury promotes alveolar repair and reduces fibrosis. Thus, targeting of a maladapted hematopoietic-vascular niche, in which macrophages, PCECs and perivascular fibroblasts interact, may help to develop therapy to spur lung regeneration and alleviate fibrosis., The lung, which facilitates oxygen exchange and defends against inhaled toxicants, is frequently exposed to infectious or noxious injury. Injured lungs can undergo facultative regeneration to restore alveolar architecture and [...]

Published
2016
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