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Article: The GPCR properties of polycystin-1- A new paradigm.

Maser, Robin L / Calvet, James P / Parnell, Stephen C

2022 Volume 9, Page(s) 1035507

Abstract: Polycystin-1 (PC1) is an 11-transmembrane (TM) domain-containing protein encoded by ... ...

Abstract	Polycystin-1 (PC1) is an 11-transmembrane (TM) domain-containing protein encoded by the
Language	English
Publishing date	2022-11-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2022.1035507
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Article ; Online: Adhesion GPCRs as a paradigm for understanding polycystin-1 G protein regulation.

Maser, Robin L / Calvet, James P

Cellular signalling

2020 Volume 72, Page(s) 109637

Abstract: Polycystin-1, whose mutation is the most frequent cause of autosomal dominant polycystic kidney disease, is an extremely large and multi-faceted membrane protein whose primary or proximal cyst-preventing function remains undetermined. Accumulating ... ...

Abstract	Polycystin-1, whose mutation is the most frequent cause of autosomal dominant polycystic kidney disease, is an extremely large and multi-faceted membrane protein whose primary or proximal cyst-preventing function remains undetermined. Accumulating evidence supports the idea that modulation of cellular signaling by heterotrimeric G proteins is a critical function of polycystin-1. The presence of a cis-autocatalyzed, G protein-coupled receptor (GPCR) proteolytic cleavage site, or GPS, in its extracellular N-terminal domain immediately preceding the first transmembrane domain is one of the notable conserved features of the polycystin-1-like protein family, and also of the family of cell adhesion GPCRs. Adhesion GPCRs are one of five families within the GPCR superfamily and are distinguished by a large N-terminal extracellular region consisting of multiple adhesion modules with a GPS-containing GAIN domain and bimodal functions in cell adhesion and signal transduction. Recent advances from studies of adhesion GPCRs provide a new paradigm for unraveling the mechanisms by which polycystin-1-associated G protein signaling contributes to the pathogenesis of polycystic kidney disease. This review highlights the structural and functional features shared by polycystin-1 and the adhesion GPCRs and discusses the implications of such similarities for our further understanding of the functions of this complicated protein.
MeSH term(s)	Animals ; Cell Adhesion ; GTP-Binding Proteins/metabolism ; Humans ; Models, Biological ; Receptors, G-Protein-Coupled/chemistry ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction ; TRPP Cation Channels/chemistry ; TRPP Cation Channels/metabolism
Chemical Substances	Receptors, G-Protein-Coupled ; TRPP Cation Channels ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2020-04-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2020.109637
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Article: Overexpression of SMYD3 Promotes Autosomal Dominant Polycystic Kidney Disease by Mediating Cell Proliferation and Genome Instability.

Agborbesong, Ewud / Zhou, Julie Xia / Zhang, Hongbing / Li, Linda Xiaoyan / Harris, Peter C / Calvet, James P / Li, Xiaogang

Biomedicines

2024 Volume 12, Issue 3

Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disorder worldwide and progresses to end-stage renal disease (ESRD). However, its precise mechanism is not fully understood. In recent years, epigenetic ... ...

Abstract	Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disorder worldwide and progresses to end-stage renal disease (ESRD). However, its precise mechanism is not fully understood. In recent years, epigenetic reprogramming has drawn increasing attention regarding its effect on cyst growth. However, considering the complexity of epigenetic mechanisms and the broad range of alterations of epigenetic components in ADPKD, identifying more specific epigenetic factors and understanding how they are mechanistically linked to promote cyst growth is relevant for the development of treatment for ADPKD. Here, we find that the histone methyltransferase SMYD3, which activates gene transcription via histone H3 lysine 4 trimethylation (H3K4me3), is upregulated in
Language	English
Publishing date	2024-03-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines12030603
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Article ; Online: Renal MODY-fier genes.

Calvet, James P

American journal of physiology. Renal physiology

2014 Volume 307, Issue 6, Page(s) F656–7

MeSH term(s)	Female ; Humans ; Male ; Polycystic Kidney, Autosomal Recessive/genetics ; Polycystic Kidney, Autosomal Recessive/pathology
Language	English
Publishing date	2014-09-15
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00377.2014
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Article ; Online: The GPCR properties of polycystin-1- A new paradigm

Robin L. Maser / James P. Calvet / Stephen C. Parnell

Frontiers in Molecular Biosciences, Vol

2022 Volume 9

Abstract: Polycystin-1 (PC1) is an 11-transmembrane (TM) domain-containing protein encoded by the PKD1 gene, the most frequently mutated gene leading to autosomal dominant polycystic kidney disease (ADPKD). This large (> 462 kDal) protein has a complex ... ...

Abstract	Polycystin-1 (PC1) is an 11-transmembrane (TM) domain-containing protein encoded by the PKD1 gene, the most frequently mutated gene leading to autosomal dominant polycystic kidney disease (ADPKD). This large (> 462 kDal) protein has a complex posttranslational maturation process, with over five proteolytic cleavages having been described, and is found at multiple cellular locations. The initial description of the binding and activation of heterotrimeric Gαi/o by the juxtamembrane region of the PC1 cytosolic C-terminal tail (C-tail) more than 20 years ago opened the door to investigations, and controversies, into PC1’s potential function as a novel G protein-coupled receptor (GPCR). Subsequent biochemical and cellular-based assays supported an ability of the PC1 C-tail to bind numerous members of the Gα protein family and to either inhibit or activate G protein-dependent pathways involved in the regulation of ion channel activity, transcription factor activation, and apoptosis. More recent work has demonstrated an essential role for PC1-mediated G protein regulation in preventing kidney cyst development; however, the mechanisms by which PC1 regulates G protein activity continue to be discovered. Similarities between PC1 and the adhesion class of 7-TM GPCRs, most notably a conserved GPCR proteolysis site (GPS) before the first TM domain, which undergoes autocatalyzed proteolytic cleavage, suggest potential mechanisms for PC1-mediated regulation of G protein signaling. This article reviews the evidence supporting GPCR-like functions of PC1 and their relevance to cystic disease, discusses the involvement of GPS cleavage and potential ligands in regulating PC1 GPCR function, and explores potential connections between PC1 GPCR-like activity and regulation of the channel properties of the polycystin receptor-channel complex.
Keywords	ADPKD ; polycystin-1 ; polycystin-2 ; receptor-ion channel complex ; GPS cleavage ; tethered peptide agonist ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2022-11-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Vasopressin Receptor Type-2 Mediated Signaling in Renal Cell Carcinoma Stimulates Stromal Fibroblast Activation.

Jamadar, Abeda / Dwivedi, Nidhi / Mathew, Sijo / Calvet, James P / Thomas, Sufi M / Rao, Reena

International journal of molecular sciences

2022 Volume 23, Issue 14

Abstract: Vasopressin type-2 receptor (V2R) is ectopically expressed and plays a pathogenic role in clear cell renal cell carcinoma (ccRCC) tumor cells. Here we examined how V2R signaling within human ccRCC tumor cells (Caki1 cells) stimulates stromal cancer- ... ...

Abstract	Vasopressin type-2 receptor (V2R) is ectopically expressed and plays a pathogenic role in clear cell renal cell carcinoma (ccRCC) tumor cells. Here we examined how V2R signaling within human ccRCC tumor cells (Caki1 cells) stimulates stromal cancer-associated fibroblasts (CAFs). We found that cell culture conditioned media from Caki1 cells increased activation, migration, and proliferation of fibroblasts in vitro, which was inhibited by V2R gene silencing in Caki1 cells. Analysis of the conditioned media and mRNA of the V2R gene silenced and control Caki1 cells showed that V2R regulates the production of CAF-activating factors. Some of these factors were also found to be regulated by YAP in these Caki1 cells. YAP expression colocalized and correlated with V2R expression in ccRCC tumor tissue. V2R gene silencing or V2R antagonist significantly reduced YAP in Caki1 cells. Moreover, the V2R antagonist reduced YAP expression and myofibroblasts in mouse xenograft tumors. These results suggest that V2R plays an important role in secreting pro-fibrotic factors that stimulate fibroblast activation by a YAP-dependent mechanism in ccRCC tumors. Our results demonstrate a novel role for the V2R-YAP axis in the regulation of myofibroblasts in ccRCC and a potential therapeutic target.
MeSH term(s)	Animals ; Antidiuretic Hormone Receptor Antagonists/pharmacology ; Cancer-Associated Fibroblasts/drug effects ; Cancer-Associated Fibroblasts/metabolism ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/metabolism ; Carcinoma, Renal Cell/pathology ; Cell Line, Tumor ; Culture Media, Conditioned ; Fibroblasts/metabolism ; Humans ; Kidney/drug effects ; Kidney/metabolism ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/pathology ; Mice ; Receptors, Vasopressin/genetics ; Receptors, Vasopressin/metabolism ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/physiology ; Vasopressins/genetics ; Vasopressins/metabolism ; Xenograft Model Antitumor Assays
Chemical Substances	Antidiuretic Hormone Receptor Antagonists ; Culture Media, Conditioned ; Receptors, Vasopressin ; Vasopressins (11000-17-2)
Language	English
Publishing date	2022-07-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23147601
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Article ; Online: Prdx5 regulates DNA damage response through autophagy-dependent Sirt2-p53 axis.

Agborbesong, Ewud / Zhou, Julie X / Li, Linda X / Harris, Peter C / Calvet, James P / Li, Xiaogang

Human molecular genetics

2022 Volume 32, Issue 4, Page(s) 567–579

Abstract: DNA damage response (DDR) is an important signaling-transduction network that promotes the repair of DNA lesions which can induce and/or support diseases. However, the mechanisms involved in its regulation are not fully understood. Recent studies suggest ...

Abstract	DNA damage response (DDR) is an important signaling-transduction network that promotes the repair of DNA lesions which can induce and/or support diseases. However, the mechanisms involved in its regulation are not fully understood. Recent studies suggest that the peroxiredoxin 5 (Prdx5) enzyme, which detoxifies reactive oxygen species, is associated to genomic instability and signal transduction. Its role in the regulation of DDR, however, is not well characterized. In this study, we demonstrate a role of Prdx5 in the regulation of the DDR signaling pathway. Knockdown of Prdx5 resulted in DNA damage manifested by the induction of phosphorylated histone H2AX (γ-H2AX) and p53-binding protein 1 (53BP1). We show that Prdx5 regulates DDR through (1) polo-like kinase 1 (Plk1) mediated phosphorylation of ataxia telangiectasia mutated (ATM) kinase to further trigger downstream mediators Chek1 and Chek2; (2) the increase of the acetylation of p53 at lysine 382, stabilizing p53 in the nucleus and enhancing transcription and (3) the induction of autophagy, which regulates the recycling of molecules involved in DDR. We identified Sirt2 as a novel deacetylase of p53 at lysine 382, and Sirt2 regulated the acetylation status of p53 at lysine 382 in a Prdx5-dependent manner. Furthermore, we found that exogenous expression of Prdx5 decreased DNA damage and the activation of ATM in Pkd1 mutant renal epithelial cells, suggesting that Prdx5 may play a protective role from DNA damage in cystic renal epithelial cells. This study identified a novel mechanism of Prdx5 in the regulation of DDR through the ATM/p53/Sirt2 signaling cascade.
MeSH term(s)	Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Histones/metabolism ; Peroxiredoxins/genetics ; Sirtuin 2/metabolism ; Lysine/genetics ; Ataxia Telangiectasia Mutated Proteins/genetics ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Cell Cycle Proteins/genetics ; Phosphorylation ; DNA Damage
Chemical Substances	Tumor Suppressor Protein p53 ; Histones ; Peroxiredoxins (EC 1.11.1.15) ; Sirtuin 2 (EC 3.5.1.-) ; Lysine (K3Z4F929H6) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Cell Cycle Proteins
Language	English
Publishing date	2022-09-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddac218
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Zs.A 3469: Show issues

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Article ; Online: Polycystin-1 Interacting Protein-1 (CU062) Interacts with the Ectodomain of Polycystin-1 (PC1).

Lea, Wendy A / Winklhofer, Thomas / Zelenchuk, Lesya / Sharma, Madhulika / Rossol-Allison, Jessica / Fields, Timothy A / Reif, Gail / Calvet, James P / Bakeberg, Jason L / Wallace, Darren P / Ward, Christopher J

Cells

2023 Volume 12, Issue 17

Abstract: ... ...

Abstract	The
MeSH term(s)	Humans ; Extracellular Vesicles ; Genes, Regulator ; Mitochondria ; Polycystic Kidney, Autosomal Dominant ; TRPP Cation Channels
Chemical Substances	TRPP Cation Channels ; polycystic kidney disease 1 protein
Language	English
Publishing date	2023-08-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12172166
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Article: Metanephric organ culture.

Maser, Robin L / Magenheimer, Brenda S / Calvet, James P

Methods in cell biology

2019 Volume 153, Page(s) 169–183

Abstract: Metanephric organ culture, or ex vivo embryonic kidney culture, was developed in the mid-twentieth century as a means to understand the development of the mammalian kidney and was used in early studies of polycystic kidney disease to explore mechanisms ... ...

Abstract	Metanephric organ culture, or ex vivo embryonic kidney culture, was developed in the mid-twentieth century as a means to understand the development of the mammalian kidney and was used in early studies of polycystic kidney disease to explore mechanisms of renal cyst initiation by non-genetic factors. Following the identification of cystogenic genes, a resurgence of the use of metanephric organ culture occurred and has yielded insight into basic mechanisms of cystic dilation; facilitated identification of pathogenic pathways and potential therapeutic targets; and provided a system for evaluating therapeutic agents. This chapter provides detailed, step-by-step protocols with rationale and tips for the establishment, maintenance and treatment of metanephric organ cultures, and for performance of the most commonly employed secondary analyses of these cultures.
MeSH term(s)	Animals ; Culture Media/metabolism ; Cyclic AMP/metabolism ; Disease Models, Animal ; Embryo, Mammalian ; Female ; Humans ; Intravital Microscopy/instrumentation ; Intravital Microscopy/methods ; Kidney ; Mice ; Microdissection/instrumentation ; Microdissection/methods ; Microscopy, Fluorescence/instrumentation ; Microscopy, Fluorescence/methods ; Organ Culture Techniques/methods ; Polycystic Kidney Diseases/pathology
Chemical Substances	Culture Media ; Cyclic AMP (E0399OZS9N)
Language	English
Publishing date	2019-06-13
Publishing country	United States
Document type	Journal Article
ISSN	0091-679X
ISSN	0091-679X
DOI	10.1016/bs.mcb.2019.04.018
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Article ; Online: Single-Cell and CellChat Resolution Identifies Collecting Duct Cell Subsets and Their Communications with Adjacent Cells in PKD Kidneys.

Li, Linda Xiaoyan / Zhang, Xu / Zhang, Hongbing / Agborbesong, Ewud / Zhou, Julie Xia / Calvet, James P / Li, Xiaogang

Cells

2022 Volume 12, Issue 1

Abstract: ADPKD is a genetic disorder with a molecular complexity that remains poorly understood. In this study, we sampled renal cells to construct a comprehensive and spatiotemporally resolved gene expression atlas in ... ...

Abstract	ADPKD is a genetic disorder with a molecular complexity that remains poorly understood. In this study, we sampled renal cells to construct a comprehensive and spatiotemporally resolved gene expression atlas in whole
MeSH term(s)	Mice ; Animals ; Polycystic Kidney, Autosomal Dominant/genetics ; Kidney/metabolism ; Polycystic Kidney Diseases/metabolism ; Epithelial Cells/metabolism
Language	English
Publishing date	2022-12-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12010045
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