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  1. Article ; Online: Polycystin-2 in the Endoplasmic Reticulum: Bending Ideas about the Role of the Cilium.

    Caplan, Michael J

    Journal of the American Society of Nephrology : JASN

    2022  Volume 33, Issue 8, Page(s) 1433–1434

    MeSH term(s) Calcium/metabolism ; Cilia/metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Polycystic Kidney, Autosomal Dominant ; TRPP Cation Channels/genetics
    Chemical Substances TRPP Cation Channels ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-07-23
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2022050557
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3344: Show issues Location:
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  2. Article: AMPK and Polycystic Kidney Disease Drug Development: An Interesting Off-Target Target.

    Caplan, Michael J

    Frontiers in medicine

    2022  Volume 9, Page(s) 753418

    Abstract: Autosomal Dominant Polycystic Kidney Disease is a genetic disease that causes dramatic perturbations of both renal tissue architecture and of a multitude of cellular signaling pathways. The relationship between the products of the genes whose mutations ... ...

    Abstract Autosomal Dominant Polycystic Kidney Disease is a genetic disease that causes dramatic perturbations of both renal tissue architecture and of a multitude of cellular signaling pathways. The relationship between the products of the genes whose mutations cause polycystic kidney disease and these signaling pathways remains difficult to determine. It is clear, however, that cellular metabolism is dramatically altered in cells that are affected by polycystic kidney disease mutations. Adenosine monophosphate-stimulated protein kinase is a master regulator of cellular energy use and generation pathways whose activity appears to be perturbed in cells affected by polycystic kidney disease. Furthermore, modulation of this enzyme's activity may constitute a promising approach for the development of new therapeutics for polycystic kidney disease.
    Language English
    Publishing date 2022-01-31
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2022.753418
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  3. Article ; Online: Physiology and

    J Caplan, Michael

    Physiology (Bethesda, Md.)

    2021  Volume 36, Issue 5, Page(s) 268–269

    Language English
    Publishing date 2021-08-04
    Publishing country United States
    Document type Editorial
    ZDB-ID 2158667-6
    ISSN 1548-9221 ; 1548-9213
    ISSN (online) 1548-9221
    ISSN 1548-9213
    DOI 10.1152/physiol.00015.2021
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  4. Article ; Online: AMPK and Polycystic Kidney Disease Drug Development

    Michael J. Caplan

    Frontiers in Medicine, Vol

    An Interesting Off-Target Target

    2022  Volume 9

    Abstract: Autosomal Dominant Polycystic Kidney Disease is a genetic disease that causes dramatic perturbations of both renal tissue architecture and of a multitude of cellular signaling pathways. The relationship between the products of the genes whose mutations ... ...

    Abstract Autosomal Dominant Polycystic Kidney Disease is a genetic disease that causes dramatic perturbations of both renal tissue architecture and of a multitude of cellular signaling pathways. The relationship between the products of the genes whose mutations cause polycystic kidney disease and these signaling pathways remains difficult to determine. It is clear, however, that cellular metabolism is dramatically altered in cells that are affected by polycystic kidney disease mutations. Adenosine monophosphate-stimulated protein kinase is a master regulator of cellular energy use and generation pathways whose activity appears to be perturbed in cells affected by polycystic kidney disease. Furthermore, modulation of this enzyme's activity may constitute a promising approach for the development of new therapeutics for polycystic kidney disease.
    Keywords Autosomal Dominant Polycystic Kidney Disease ; adenosine monophosphate-stimulated protein kinase ; metabolism ; mTOR ; CFTR ; metformin ; Medicine (General) ; R5-920
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Calcium signalling and transport in the kidney.

    Staruschenko, Alexander / Alexander, R Todd / Caplan, Michael J / Ilatovskaya, Daria V

    Nature reviews. Nephrology

    2024  

    Abstract: The kidney plays a pivotal role in regulating calcium levels within the body. Approximately 98% of the filtered calcium is reabsorbed in the nephron, and this process is tightly controlled to maintain calcium homeostasis, which is required to facilitate ... ...

    Abstract The kidney plays a pivotal role in regulating calcium levels within the body. Approximately 98% of the filtered calcium is reabsorbed in the nephron, and this process is tightly controlled to maintain calcium homeostasis, which is required to facilitate optimal bone mineralization, preserve serum calcium levels within a narrow range, and support intracellular signalling mechanisms. The maintenance of these functions is attributed to a delicate balance achieved by various calcium channels, transporters, and calcium-binding proteins in renal cells. Perturbation of this balance due to deficiency or dysfunction of calcium channels and calcium-binding proteins can lead to severe complications. For example, polycystic kidney disease is linked to aberrant calcium transport and signalling. Furthermore, dysregulation of calcium levels can promote the formation of kidney stones. This Review provides an updated description of the key aspects of calcium handling in the kidney, focusing on the function of various calcium channels and the physiological stimuli that control these channels or are communicated through them. A discussion of the role of calcium as an intracellular second messenger and the pathophysiology of renal calcium dysregulation, as well as a summary of gaps in knowledge and future prospects, are also included.
    Language English
    Publishing date 2024-04-19
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/s41581-024-00835-z
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  6. Article: Heparan Sulfate: A Regulator of White Adipocyte Differentiation and of Vascular/Adipocyte Interactions.

    Sorrell, J Michael / Caplan, Arnold I

    Biomedicines

    2022  Volume 10, Issue 9

    Abstract: White adipose tissues are major endocrine organs that release factors, termed adipokines, which affect other major organ systems. The development and functions of adipose tissues depend largely upon the glycosaminoglycan heparan sulfate. Heparan sulfate ... ...

    Abstract White adipose tissues are major endocrine organs that release factors, termed adipokines, which affect other major organ systems. The development and functions of adipose tissues depend largely upon the glycosaminoglycan heparan sulfate. Heparan sulfate proteoglycans (HSPGs) surround both adipocytes and vascular structures and facilitate the communication between these two components. This communication mediates the continued export of adipokines from adipose tissues. Heparan sulfates regulate cellular physiology and communication through a sulfation code that ionically interacts with heparan-binding regions on a select set of proteins. Many of these proteins are growth factors and chemokines that regulate tissue function and inflammation. Cells regulate heparan sulfate sulfation through the release of heparanases and sulfatases. It is now possible to tissue engineer vascularized adipose tissues that express heparan sulfate proteoglycans. This makes it possible to use these tissue constructs to study the role of heparan sulfates in the regulation of adipokine production and release. It is possible to regulate the production of heparanases and sulfatases in order to fine-tune experimental studies.
    Language English
    Publishing date 2022-08-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines10092115
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  7. Article ; Online: Holding open the door reveals a new view of polycystin channel function.

    Caplan, Michael J

    EMBO reports

    2019  Volume 20, Issue 11, Page(s) e49156

    Abstract: The functions of polycystin 1 and polycystin 2 (PC1 and PC2) have been surprisingly difficult to establish. PC1 and PC2 are encoded by the Pkd1 and Pkd2 genes that are implicated in autosomal dominant polycystic kidney disease (ADPKD). ADPKD is the most ... ...

    Abstract The functions of polycystin 1 and polycystin 2 (PC1 and PC2) have been surprisingly difficult to establish. PC1 and PC2 are encoded by the Pkd1 and Pkd2 genes that are implicated in autosomal dominant polycystic kidney disease (ADPKD). ADPKD is the most common potentially lethal genetic disorder, affecting ~1 in 1,000 people. Over the course of decades, ADPKD patients' kidneys acquire numerous fluid-filled cysts whose expansion compresses the surrounding parenchyma, leading to end-stage renal disease in ~50% of afflicted individuals [1]. Identification of the genes encoding the PC proteins 20 years ago led to the hypothesis that they form an ion channel, since the sequence of PC2 marks it as a member of the TRP family of cation channels. In the ensuing 2 decades, tremendous effort has been devoted to determining whether this is indeed true and, if so, what characteristics that channel might manifest. A recent paper by Wang et al in this issue of EMBO Reports [2] demonstrates that assembly with PC1 changes the properties of the polycystin channel in ways that may help explain the complex behaviors that have been attributed to it.
    MeSH term(s) Humans ; Ion Channels ; Polycystic Kidney, Autosomal Dominant ; Signal Transduction ; TRPP Cation Channels
    Chemical Substances Ion Channels ; TRPP Cation Channels ; polycystic kidney disease 1 protein
    Language English
    Publishing date 2019-09-26
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.201949156
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    Zs.A 5433: Show issues Location:
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  8. Article ; Online: Temporal expression of Laminin-111 in the developing rat larynx.

    Caplan, Ian F / Hernandez-Morato, Ignacio / Pitman, Michael J

    Neuroscience letters

    2022  Volume 781, Page(s) 136658

    Abstract: Laminin-111 is a basement membrane protein that participates in motor innervation and reinnervation. During axonal pathfinding, laminin-111 interacts with netrin-1 (NTN1) and changes its attractant growth cone properties into repulsion. While previous ... ...

    Abstract Laminin-111 is a basement membrane protein that participates in motor innervation and reinnervation. During axonal pathfinding, laminin-111 interacts with netrin-1 (NTN1) and changes its attractant growth cone properties into repulsion. While previous models of recurrent laryngeal nerve (RLN) transection show increased Laminin-111 and NTN1 production after injury, developmental expression in the larynx has not been defined. This study investigates the expression of laminin-111 in laryngeal muscles during primary laryngeal innervation of Sprague Dawley rats. Adult larynges and embryos were sectioned for immunohistochemistry with βIII-Tubulin, laminin subunit α-1 (LAMA1), NTN1, and α-bungarotoxin. Sections were processed for single-molecule inexpensive RNA fluorescence in situ hybridization analysis of LAMA1 mRNA. LAMA1 expression increased in all intrinsic laryngeal muscles, except the medial thyroarytenoid (MTA), at E20.5. At E20.5 there was increased expression in the lateral thyroarytenoid (LTA) and posterior cricoarytenoid (PCA) compared to the MTA. NTN1 upregulation was limited to the LTA and lateral cricoarytenoid (LCA) at E16.5 without any increase in the MTA or PCA. LAMA1 and NTN1 expression did not strictly follow expected patterns relative to the known timing of innervation and does not appear to be acting similarly to its role following RLN injury. These differences between developmental and post-injury innervation provide targets for investigations of therapeutics after nerve injury.
    MeSH term(s) Animals ; Disease Models, Animal ; In Situ Hybridization, Fluorescence ; Laminin/biosynthesis ; Laminin/metabolism ; Laryngeal Muscles/growth & development ; Laryngeal Muscles/innervation ; Laryngeal Muscles/metabolism ; Nerve Regeneration/physiology ; Netrin-1/metabolism ; Pemetrexed/metabolism ; Rats ; Rats, Sprague-Dawley ; Recurrent Laryngeal Nerve Injuries/metabolism ; Recurrent Laryngeal Nerve Injuries/pathology
    Chemical Substances Laminin ; Ntn1 protein, rat ; Pemetrexed (04Q9AIZ7NO) ; Netrin-1 (158651-98-0)
    Language English
    Publishing date 2022-04-25
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 194929-9
    ISSN 1872-7972 ; 0304-3940
    ISSN (online) 1872-7972
    ISSN 0304-3940
    DOI 10.1016/j.neulet.2022.136658
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  9. Article ; Online: The tail of polycystin-1 pays the kidney a complement.

    Caplan, Michael J

    American journal of physiology. Renal physiology

    2016  Volume 310, Issue 11, Page(s) F1180–1

    MeSH term(s) Complement System Proteins ; Humans ; Kidney ; Polycystic Kidney, Autosomal Dominant ; TRPP Cation Channels
    Chemical Substances TRPP Cation Channels ; Complement System Proteins (9007-36-7)
    Language English
    Publishing date 2016--01
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00141.2016
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  10. Article ; Online: 2016 Robert W. Berliner Award for Excellence in Renal Physiology.

    Caplan, Michael J

    American journal of physiology. Renal physiology

    2016  Volume 310, Issue 8, Page(s) F803–F804

    MeSH term(s) Awards and Prizes ; History, 21st Century ; Humans ; Research ; Societies, Scientific ; Urinary Tract Physiological Phenomena
    Language English
    Publishing date 2016--15
    Publishing country United States
    Document type Biography ; Editorial ; Historical Article
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00128.2016
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