Special Issue "Transient Receptor Potential (TRP) Channels"
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (28 February 2014)
Dr. Loren W. Runnels
Department of Pharmacology, Rutgers Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854, USA
Interests: TRPM6 and TRPM7 ion channels; cell migration; development
Since the original cloning of the transient receptor potential (TRP) ion channel by Montell and Rubin in Drosophila melanogaster in 1989, the TRP ion channel family has grown to encompass seven subfamilies linked together primarily by their sequence homology: TRPC (“canonical”), TRPM (“melastatin”), TRPV (“vanilloid”), TRPA (“ankyrin”), TRPML (“mucolipin”), TRPP (or PKD for “polycystin”), and TRPN (“NOMPC-like”), which is only found in invertebrates and fish. TRP ion channels are widely expressed in many tissues and cell types, and have been shown to affect a broad range of cellular processes, including cell division, cell migration, and stress responses. These ion channels are also involved in the ability of cells to sense and respond to external stimuli, such as temperature, pH, and osmolarity. When activated, most TRP channels conduct cations to depolarize cells, so as to initiate a plethora of cellular responses. However, recent research has revealed important new functions for TRP ion channels in intracellular compartments. This Special Issue will provide an opportunity to publish open access research work and review articles related to the TRP channel family, and will offer comprehensive new insights into current developments within this exciting and important research field.
Dr. Loren W. Runnels
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed Open Access quarterly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 500 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
- ion channel
- cellular regulation
- signal transduction
Cells 2014, 3(3), 751-777; doi:10.3390/cells3030751 (doi registration under processing)
Received: 10 March 2014; in revised form: 15 July 2014 / Accepted: 15 July 2014 / Published: 30 July 2014| PDF Full-text (1104 KB) | HTML Full-text | XML Full-text
Cells 2014, 3(3), 662-673; doi:10.3390/cells3030662
Received: 5 May 2014; in revised form: 9 June 2014 / Accepted: 17 June 2014 / Published: 26 June 2014| PDF Full-text (409 KB) | HTML Full-text | XML Full-text
Correction: Correction: Liberati, S., et al. Loss of TRPV2 Homeostatic Control of Cell Proliferation Drives Tumor Progression. Cells 2014, 3, 112–128
Cells 2014, 3(2), 660-661; doi:10.3390/cells3020660
Received: 12 June 2014; Accepted: 16 June 2014 / Published: 20 June 2014| PDF Full-text (113 KB) | HTML Full-text | XML Full-text
Article: Unique Responses are Observed in Transient Receptor Potential Ankyrin 1 and Vanilloid 1 (TRPA1 and TRPV1) Co-Expressing Cells
Cells 2014, 3(2), 616-626; doi:10.3390/cells3020616
Received: 4 April 2014; in revised form: 29 May 2014 / Accepted: 30 May 2014 / Published: 11 June 2014| PDF Full-text (412 KB) | HTML Full-text | XML Full-text
Cells 2014, 3(2), 517-545; doi:10.3390/cells3020517
Received: 27 March 2014; in revised form: 14 May 2014 / Accepted: 15 May 2014 / Published: 23 May 2014| PDF Full-text (657 KB) | HTML Full-text | XML Full-text
Article: Aberrantly Over-Expressed TRPM8 Channels in Pancreatic Adenocarcinoma: Correlation with Tumor Size/Stage and Requirement for Cancer Cells Invasion
Cells 2014, 3(2), 500-516; doi:10.3390/cells3020500
Received: 10 March 2014; in revised form: 7 May 2014 / Accepted: 14 May 2014 / Published: 23 May 2014| PDF Full-text (1463 KB) | HTML Full-text | XML Full-text
Cells 2014, 3(2), 455-475; doi:10.3390/cells3020455
Received: 21 March 2014; in revised form: 22 April 2014 / Accepted: 13 May 2014 / Published: 21 May 2014| PDF Full-text (387 KB) | HTML Full-text | XML Full-text
Review: TRP Channels Involved in Spontaneous L-Glutamate Release Enhancement in the Adult Rat Spinal Substantia Gelatinosa
Cells 2014, 3(2), 331-362; doi:10.3390/cells3020331
Received: 28 February 2014; in revised form: 10 April 2014 / Accepted: 18 April 2014 / Published: 29 April 2014| PDF Full-text (2462 KB) | HTML Full-text | XML Full-text
Cells 2014, 3(2), 288-303; doi:10.3390/cells3020288
Received: 28 February 2014; in revised form: 29 March 2014 / Accepted: 2 April 2014 / Published: 9 April 2014| PDF Full-text (658 KB) | HTML Full-text | XML Full-text
Cells 2014, 3(2), 258-287; doi:10.3390/cells3020258
Received: 28 February 2014; in revised form: 25 March 2014 / Accepted: 27 March 2014 / Published: 8 April 2014| PDF Full-text (1325 KB) | HTML Full-text | XML Full-text
Cells 2014, 3(2), 247-257; doi:10.3390/cells3020247
Received: 18 February 2014; in revised form: 17 March 2014 / Accepted: 25 March 2014 / Published: 4 April 2014| PDF Full-text (582 KB) | HTML Full-text | XML Full-text
Cells 2014, 3(1), 112-128; doi:10.3390/cells3010112
Received: 19 December 2013; in revised form: 22 January 2014 / Accepted: 8 February 2014 / Published: 19 February 2014| Cited by 1 | PDF Full-text (297 KB) | HTML Full-text | XML Full-text | Correction
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of Paper: Review
Title: Classical transient receptor potential 1 (TRPC1): Channel or Channel regulator?
Authors: Alexander Dietrich and Thomas Gudermann
Affiliations: Walther-Straub-Institute of Pharmacology and Toxicology, LM-University Munich, Nussbaumstr. 26, D-80336 Munich, Germany; E-Mail: firstname.lastname@example.org
Abstract: In contrast to other TRPC channels the function of TRPC1 as an ion channel is a matter of debate, because it is difficult to obtain substantial functional signals over background in response to over-expression of TRPC1 alone. Along these lines, heterologously expressed TRPC1 is poorly translocated as a homotetramer to the plasma membrane and may not act physiologically on its own, but is rather an important linker and regulator protein in other functional heteromeric TRPC channel tetramers. However, due to the lack of highly specific TRPC1 antibodies which detect native TRPC1 channels in primary cells identification of functional TRPC1-containing heteromeric TRPC channel complexes in the plasma membrane is still challenging. This review will give an overview on the current status of research on TRPC1 function in cells using pharmacological and genetic tools like TRPC1 deficient mouse models. Type of Paper: Review
Type of the Paper: Review
Title: Natural and synthetic modulators of TRPM7
Authors: Sebastian Schäfer, Vladimir Chubanov, and Thomas Gudermann *
Affiliations: Walther-Straub-Institute of Pharmacology and Toxicology, University of Munich, Goethestrasse 33, 80336 Munich, Germany; E-Mail: email@example.com
Abstract: Transient receptor potential cation channel subfamily M member 7 (TRPM7) is a bi-functional protein comprising a TRP ion channel segment linked to an α-type protein kinase domain. TRPM7 is essential for proliferation and cell growth. TRPM7 was found to be associated with anoxic neuronal death, cardiac fibrosis and tumor cell proliferation and other pathophysiological processes. Despite the physiological and clinical importance of TRPM7, only a few exogenous modulators of TRPM7 channel are currently available. Recently, independent laboratories identified several small organic compounds enabling to modulate TRPM7 channel activity. Here, we provide a concise overview of this emerging field.
Last update: 10 June 2014