Tissue Specificity: Store-Operated Ca2+ Entry in Cardiac Myocytes View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2017-09-13

AUTHORS

Martin D. Bootman , Katja Rietdorf

ABSTRACT

Calcium (Ca2+) is a key regulator of cardiomyocyte contraction. The Ca2+ channels, pumps, and exchangers responsible for the cyclical cytosolic Ca2+ signals that underlie contraction are well known. In addition to those Ca2+ signaling components responsible for contraction, it has been proposed that cardiomyocytes express channels that promote the influx of Ca2+ from the extracellular milieu to the cytosol in response to depletion of intracellular Ca2+ stores. With non-excitable cells, this store-operated Ca2+ entry (SOCE) is usually easily demonstrated and is essential for prolonging cellular Ca2+ signaling and for refilling depleted Ca2+ stores. The role of SOCE in cardiomyocytes, however, is rather more elusive. While there is published evidence for increased Ca2+ influx into cardiomyocytes following Ca2+ store depletion, it has not been universally observed. Moreover, SOCE appears to be prominent in embryonic cardiomyocytes but declines with postnatal development. In contrast, there is overwhelming evidence that the molecular components of SOCE (e.g., STIM, Orai, and TRPC proteins) are expressed in cardiomyocytes from embryo to adult. Moreover, these proteins have been shown to contribute to disease conditions such as pathological hypertrophy, and reducing their expression can attenuate hypertrophic growth. It is plausible that SOCE might underlie Ca2+ influx into cardiomyocytes and may have important signaling functions perhaps by activating local Ca2+-sensitive processes. However, the STIM, Orai, and TRPC proteins appear to cooperate with multiple protein partners in signaling complexes. It is therefore possible that some of their signaling activities are not mediated by Ca2+ influx signals, but by protein-protein interactions. More... »

PAGES

363-387

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-319-57732-6_19

DOI

http://dx.doi.org/10.1007/978-3-319-57732-6_19

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1091605275

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28900924


Indexing Status Check whether this publication has been indexed by Scopus and Web Of Science using the SN Indexing Status Tool
Incoming Citations Browse incoming citations for this publication using opencitations.net

JSON-LD is the canonical representation for SciGraph data.

TIP: You can open this SciGraph record using an external JSON-LD service: JSON-LD Playground Google SDTT

[
  {
    "@context": "https://springernature.github.io/scigraph/jsonld/sgcontext.json", 
    "about": [
      {
        "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/11", 
        "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
        "name": "Medical and Health Sciences", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Animals", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Calcium", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Calcium Channels", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Calcium Signaling", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Humans", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Myocytes, Cardiac", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Organ Specificity", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Stromal Interaction Molecules", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "TRPC Cation Channels", 
        "type": "DefinedTerm"
      }
    ], 
    "author": [
      {
        "affiliation": {
          "alternateName": "School of Life, Health and Chemical Sciences, The Open University, Walton Hall, MK7 6AA, Milton Keynes, UK", 
          "id": "http://www.grid.ac/institutes/grid.10837.3d", 
          "name": [
            "School of Life, Health and Chemical Sciences, The Open University, Walton Hall, MK7 6AA, Milton Keynes, UK"
          ], 
          "type": "Organization"
        }, 
        "familyName": "Bootman", 
        "givenName": "Martin D.", 
        "id": "sg:person.01241632256.55", 
        "sameAs": [
          "https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01241632256.55"
        ], 
        "type": "Person"
      }, 
      {
        "affiliation": {
          "alternateName": "School of Life, Health and Chemical Sciences, The Open University, Walton Hall, MK7 6AA, Milton Keynes, UK", 
          "id": "http://www.grid.ac/institutes/grid.10837.3d", 
          "name": [
            "School of Life, Health and Chemical Sciences, The Open University, Walton Hall, MK7 6AA, Milton Keynes, UK"
          ], 
          "type": "Organization"
        }, 
        "familyName": "Rietdorf", 
        "givenName": "Katja", 
        "id": "sg:person.0740670530.33", 
        "sameAs": [
          "https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.0740670530.33"
        ], 
        "type": "Person"
      }
    ], 
    "datePublished": "2017-09-13", 
    "datePublishedReg": "2017-09-13", 
    "description": "Calcium (Ca2+) is a key regulator of cardiomyocyte contraction. The Ca2+ channels, pumps, and exchangers responsible for the cyclical cytosolic Ca2+ signals that underlie contraction are well known. In addition to those Ca2+ signaling components responsible for contraction, it has been proposed that cardiomyocytes express channels that promote the influx of Ca2+ from the extracellular milieu to the cytosol in response to depletion of intracellular Ca2+ stores. With non-excitable cells, this store-operated Ca2+ entry (SOCE) is usually easily demonstrated and is essential for prolonging cellular Ca2+ signaling and for refilling depleted Ca2+ stores. The role of SOCE in cardiomyocytes, however, is rather more elusive. While there is published evidence for increased Ca2+ influx into cardiomyocytes following Ca2+ store depletion, it has not been universally observed. Moreover, SOCE appears to be prominent in embryonic cardiomyocytes but declines with postnatal development. In contrast, there is overwhelming evidence that the molecular components of SOCE (e.g., STIM, Orai, and TRPC proteins) are expressed in cardiomyocytes from embryo to adult. Moreover, these proteins have been shown to contribute to disease conditions such as pathological hypertrophy, and reducing their expression can attenuate hypertrophic growth. It is plausible that SOCE might underlie Ca2+ influx into cardiomyocytes and may have important signaling functions perhaps by activating local Ca2+-sensitive processes. However, the STIM, Orai, and TRPC proteins appear to cooperate with multiple protein partners in signaling complexes. It is therefore possible that some of their signaling activities are not mediated by Ca2+ influx signals, but by protein-protein interactions.", 
    "editor": [
      {
        "familyName": "Groschner", 
        "givenName": "Klaus", 
        "type": "Person"
      }, 
      {
        "familyName": "Graier", 
        "givenName": "Wolfgang F.", 
        "type": "Person"
      }, 
      {
        "familyName": "Romanin", 
        "givenName": "Christoph", 
        "type": "Person"
      }
    ], 
    "genre": "chapter", 
    "id": "sg:pub.10.1007/978-3-319-57732-6_19", 
    "isAccessibleForFree": false, 
    "isPartOf": {
      "isbn": [
        "978-3-319-57731-9", 
        "978-3-319-57732-6"
      ], 
      "name": "Store-Operated Ca\u00b2\u207a Entry (SOCE) Pathways", 
      "type": "Book"
    }, 
    "keywords": [
      "role of SOCE", 
      "influx of Ca2", 
      "store-operated Ca2", 
      "pathological hypertrophy", 
      "non-excitable cells", 
      "intracellular Ca2", 
      "postnatal development", 
      "underlie contraction", 
      "cardiomyocyte contraction", 
      "cytosolic Ca2", 
      "influx signal", 
      "store depletion", 
      "cardiac myocytes", 
      "hypertrophic growth", 
      "TRPC proteins", 
      "cellular Ca2", 
      "disease conditions", 
      "cardiomyocytes", 
      "local Ca2", 
      "SOCE", 
      "embryonic cardiomyocytes", 
      "contraction", 
      "extracellular milieu", 
      "Ca2", 
      "overwhelming evidence", 
      "key regulator", 
      "influx", 
      "hypertrophy", 
      "myocytes", 
      "evidence", 
      "depletion", 
      "adults", 
      "stores", 
      "protein", 
      "calcium", 
      "Orai", 
      "signaling", 
      "entry", 
      "molecular components", 
      "cells", 
      "expression", 
      "milieu", 
      "response", 
      "STIM", 
      "decline", 
      "activity", 
      "cytosol", 
      "role", 
      "regulator", 
      "embryos", 
      "contrast", 
      "sensitive process", 
      "multiple protein partners", 
      "protein-protein interactions", 
      "function", 
      "partners", 
      "addition", 
      "development", 
      "pump", 
      "components", 
      "protein partners", 
      "growth", 
      "channels", 
      "signals", 
      "conditions", 
      "interaction", 
      "complexes", 
      "process", 
      "exchanger"
    ], 
    "name": "Tissue Specificity: Store-Operated Ca2+ Entry in Cardiac Myocytes", 
    "pagination": "363-387", 
    "productId": [
      {
        "name": "dimensions_id", 
        "type": "PropertyValue", 
        "value": [
          "pub.1091605275"
        ]
      }, 
      {
        "name": "doi", 
        "type": "PropertyValue", 
        "value": [
          "10.1007/978-3-319-57732-6_19"
        ]
      }, 
      {
        "name": "pubmed_id", 
        "type": "PropertyValue", 
        "value": [
          "28900924"
        ]
      }
    ], 
    "publisher": {
      "name": "Springer Nature", 
      "type": "Organisation"
    }, 
    "sameAs": [
      "https://doi.org/10.1007/978-3-319-57732-6_19", 
      "https://app.dimensions.ai/details/publication/pub.1091605275"
    ], 
    "sdDataset": "chapters", 
    "sdDatePublished": "2022-12-01T06:50", 
    "sdLicense": "https://scigraph.springernature.com/explorer/license/", 
    "sdPublisher": {
      "name": "Springer Nature - SN SciGraph project", 
      "type": "Organization"
    }, 
    "sdSource": "s3://com-springernature-scigraph/baseset/20221201/entities/gbq_results/chapter/chapter_299.jsonl", 
    "type": "Chapter", 
    "url": "https://doi.org/10.1007/978-3-319-57732-6_19"
  }
]
 

Download the RDF metadata as:  json-ld nt turtle xml License info

HOW TO GET THIS DATA PROGRAMMATICALLY:

JSON-LD is a popular format for linked data which is fully compatible with JSON.

curl -H 'Accept: application/ld+json' 'https://scigraph.springernature.com/pub.10.1007/978-3-319-57732-6_19'

N-Triples is a line-based linked data format ideal for batch operations.

curl -H 'Accept: application/n-triples' 'https://scigraph.springernature.com/pub.10.1007/978-3-319-57732-6_19'

Turtle is a human-readable linked data format.

curl -H 'Accept: text/turtle' 'https://scigraph.springernature.com/pub.10.1007/978-3-319-57732-6_19'

RDF/XML is a standard XML format for linked data.

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1007/978-3-319-57732-6_19'


 

This table displays all metadata directly associated to this object as RDF triples.

181 TRIPLES      22 PREDICATES      102 URIs      96 LITERALS      17 BLANK NODES

Subject Predicate Object
1 sg:pub.10.1007/978-3-319-57732-6_19 schema:about N0340a8f1511e4d10bf6896e5baf6077e
2 N16ae6f3d45cf406b87dc6a41305fd519
3 N3e5b49afd0df43c4b411694d76a9385d
4 N77fb97c97c784cf1a8853a6647c4f638
5 Na3c6fb2d721a44198fb6ca23a17195af
6 Nd460bed7409f43a1a9c8ce0ae212ef63
7 Nda3d3e16e6304df297a4b235b14b3bac
8 Ne3002fbf2a054cef9b68a8fd4c8d0a80
9 Nea411710905644c2a54fee33ab58fd13
10 anzsrc-for:11
11 schema:author N9b2c2600c5ed45efa135f9dd9ca2a45b
12 schema:datePublished 2017-09-13
13 schema:datePublishedReg 2017-09-13
14 schema:description Calcium (Ca2+) is a key regulator of cardiomyocyte contraction. The Ca2+ channels, pumps, and exchangers responsible for the cyclical cytosolic Ca2+ signals that underlie contraction are well known. In addition to those Ca2+ signaling components responsible for contraction, it has been proposed that cardiomyocytes express channels that promote the influx of Ca2+ from the extracellular milieu to the cytosol in response to depletion of intracellular Ca2+ stores. With non-excitable cells, this store-operated Ca2+ entry (SOCE) is usually easily demonstrated and is essential for prolonging cellular Ca2+ signaling and for refilling depleted Ca2+ stores. The role of SOCE in cardiomyocytes, however, is rather more elusive. While there is published evidence for increased Ca2+ influx into cardiomyocytes following Ca2+ store depletion, it has not been universally observed. Moreover, SOCE appears to be prominent in embryonic cardiomyocytes but declines with postnatal development. In contrast, there is overwhelming evidence that the molecular components of SOCE (e.g., STIM, Orai, and TRPC proteins) are expressed in cardiomyocytes from embryo to adult. Moreover, these proteins have been shown to contribute to disease conditions such as pathological hypertrophy, and reducing their expression can attenuate hypertrophic growth. It is plausible that SOCE might underlie Ca2+ influx into cardiomyocytes and may have important signaling functions perhaps by activating local Ca2+-sensitive processes. However, the STIM, Orai, and TRPC proteins appear to cooperate with multiple protein partners in signaling complexes. It is therefore possible that some of their signaling activities are not mediated by Ca2+ influx signals, but by protein-protein interactions.
15 schema:editor Nbd1c9560c87e4dccbd0382c86ff8e765
16 schema:genre chapter
17 schema:isAccessibleForFree false
18 schema:isPartOf N409818afce6349a7a32e9d62c89950a5
19 schema:keywords Ca2
20 Orai
21 SOCE
22 STIM
23 TRPC proteins
24 activity
25 addition
26 adults
27 calcium
28 cardiac myocytes
29 cardiomyocyte contraction
30 cardiomyocytes
31 cells
32 cellular Ca2
33 channels
34 complexes
35 components
36 conditions
37 contraction
38 contrast
39 cytosol
40 cytosolic Ca2
41 decline
42 depletion
43 development
44 disease conditions
45 embryonic cardiomyocytes
46 embryos
47 entry
48 evidence
49 exchanger
50 expression
51 extracellular milieu
52 function
53 growth
54 hypertrophic growth
55 hypertrophy
56 influx
57 influx of Ca2
58 influx signal
59 interaction
60 intracellular Ca2
61 key regulator
62 local Ca2
63 milieu
64 molecular components
65 multiple protein partners
66 myocytes
67 non-excitable cells
68 overwhelming evidence
69 partners
70 pathological hypertrophy
71 postnatal development
72 process
73 protein
74 protein partners
75 protein-protein interactions
76 pump
77 regulator
78 response
79 role
80 role of SOCE
81 sensitive process
82 signaling
83 signals
84 store depletion
85 store-operated Ca2
86 stores
87 underlie contraction
88 schema:name Tissue Specificity: Store-Operated Ca2+ Entry in Cardiac Myocytes
89 schema:pagination 363-387
90 schema:productId N807957a54ae248418d7cb5f97a859ec5
91 N84f4ec8351904447b52d8c425145e9e0
92 Ncbd3d65a5e4545f79c6278f57ab7ede3
93 schema:publisher Ncd3ca9ad000b4304a46aadf6130074ae
94 schema:sameAs https://app.dimensions.ai/details/publication/pub.1091605275
95 https://doi.org/10.1007/978-3-319-57732-6_19
96 schema:sdDatePublished 2022-12-01T06:50
97 schema:sdLicense https://scigraph.springernature.com/explorer/license/
98 schema:sdPublisher Ncf6270a96f0f44e8aa25c60461241b0e
99 schema:url https://doi.org/10.1007/978-3-319-57732-6_19
100 sgo:license sg:explorer/license/
101 sgo:sdDataset chapters
102 rdf:type schema:Chapter
103 N0340a8f1511e4d10bf6896e5baf6077e schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
104 schema:name Organ Specificity
105 rdf:type schema:DefinedTerm
106 N0b5df0ff6e6e4cc0ab1a81db9e395fdd schema:familyName Romanin
107 schema:givenName Christoph
108 rdf:type schema:Person
109 N16ae6f3d45cf406b87dc6a41305fd519 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
110 schema:name Myocytes, Cardiac
111 rdf:type schema:DefinedTerm
112 N3e5b49afd0df43c4b411694d76a9385d schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
113 schema:name Animals
114 rdf:type schema:DefinedTerm
115 N409818afce6349a7a32e9d62c89950a5 schema:isbn 978-3-319-57731-9
116 978-3-319-57732-6
117 schema:name Store-Operated Ca²⁺ Entry (SOCE) Pathways
118 rdf:type schema:Book
119 N77fb97c97c784cf1a8853a6647c4f638 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
120 schema:name TRPC Cation Channels
121 rdf:type schema:DefinedTerm
122 N807957a54ae248418d7cb5f97a859ec5 schema:name dimensions_id
123 schema:value pub.1091605275
124 rdf:type schema:PropertyValue
125 N84f4ec8351904447b52d8c425145e9e0 schema:name pubmed_id
126 schema:value 28900924
127 rdf:type schema:PropertyValue
128 N9b2c2600c5ed45efa135f9dd9ca2a45b rdf:first sg:person.01241632256.55
129 rdf:rest Nff5cfff474ea4fada485ac0bb7b7c046
130 Na3c6fb2d721a44198fb6ca23a17195af schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
131 schema:name Calcium Channels
132 rdf:type schema:DefinedTerm
133 Naefa4d7615764dcf824f693eac1385ab schema:familyName Groschner
134 schema:givenName Klaus
135 rdf:type schema:Person
136 Nbd1c9560c87e4dccbd0382c86ff8e765 rdf:first Naefa4d7615764dcf824f693eac1385ab
137 rdf:rest Nc090e10a6f9b47cd993ea2f6fdd97220
138 Nbd6526e53cb0475299a7c3eea2f77c89 rdf:first N0b5df0ff6e6e4cc0ab1a81db9e395fdd
139 rdf:rest rdf:nil
140 Nc090e10a6f9b47cd993ea2f6fdd97220 rdf:first Ndb809492ae2e40029b03985991a728f8
141 rdf:rest Nbd6526e53cb0475299a7c3eea2f77c89
142 Ncbd3d65a5e4545f79c6278f57ab7ede3 schema:name doi
143 schema:value 10.1007/978-3-319-57732-6_19
144 rdf:type schema:PropertyValue
145 Ncd3ca9ad000b4304a46aadf6130074ae schema:name Springer Nature
146 rdf:type schema:Organisation
147 Ncf6270a96f0f44e8aa25c60461241b0e schema:name Springer Nature - SN SciGraph project
148 rdf:type schema:Organization
149 Nd460bed7409f43a1a9c8ce0ae212ef63 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
150 schema:name Calcium
151 rdf:type schema:DefinedTerm
152 Nda3d3e16e6304df297a4b235b14b3bac schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
153 schema:name Calcium Signaling
154 rdf:type schema:DefinedTerm
155 Ndb809492ae2e40029b03985991a728f8 schema:familyName Graier
156 schema:givenName Wolfgang F.
157 rdf:type schema:Person
158 Ne3002fbf2a054cef9b68a8fd4c8d0a80 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
159 schema:name Humans
160 rdf:type schema:DefinedTerm
161 Nea411710905644c2a54fee33ab58fd13 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
162 schema:name Stromal Interaction Molecules
163 rdf:type schema:DefinedTerm
164 Nff5cfff474ea4fada485ac0bb7b7c046 rdf:first sg:person.0740670530.33
165 rdf:rest rdf:nil
166 anzsrc-for:11 schema:inDefinedTermSet anzsrc-for:
167 schema:name Medical and Health Sciences
168 rdf:type schema:DefinedTerm
169 sg:person.01241632256.55 schema:affiliation grid-institutes:grid.10837.3d
170 schema:familyName Bootman
171 schema:givenName Martin D.
172 schema:sameAs https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01241632256.55
173 rdf:type schema:Person
174 sg:person.0740670530.33 schema:affiliation grid-institutes:grid.10837.3d
175 schema:familyName Rietdorf
176 schema:givenName Katja
177 schema:sameAs https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.0740670530.33
178 rdf:type schema:Person
179 grid-institutes:grid.10837.3d schema:alternateName School of Life, Health and Chemical Sciences, The Open University, Walton Hall, MK7 6AA, Milton Keynes, UK
180 schema:name School of Life, Health and Chemical Sciences, The Open University, Walton Hall, MK7 6AA, Milton Keynes, UK
181 rdf:type schema:Organization
 




Preview window. Press ESC to close (or click here)


...