A signal for β-cell failure View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1998-02

AUTHORS

Joseph Avruch

ABSTRACT

A hallmark of human type 2 diabetes is hyperglycaemia — an excess of glucose in the bloodstream. Normally, the pancreatic β-cell compensate for this by secreting more insulin, but this fail-safe mechanism seems to malfunction in patients with the condition. Now, by generating mice that lack the insulin-receptor substrate-2 (IRS-2) gene, one group has shown that IRS-2 may be responsible for both increased insulin resistance and reduced insulin compenation. The knockout mice develop a syndrome that closely resembles human type 2 diabetes and, importantly, they have fewer β-cells than wild-type mice. More... »

PAGES

846-847

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/35998

DOI

http://dx.doi.org/10.1038/35998

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1027954810

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9495335


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/2008/06", 
        "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
        "name": "Biological Sciences", 
        "type": "DefinedTerm"
      }, 
      {
        "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"
      }, 
      {
        "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/0601", 
        "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
        "name": "Biochemistry and Cell Biology", 
        "type": "DefinedTerm"
      }, 
      {
        "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/1103", 
        "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
        "name": "Clinical Sciences", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Animals", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Diabetes Mellitus, Type 2", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Disease Models, Animal", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Humans", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Insulin Receptor Substrate Proteins", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Insulin Resistance", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Intracellular Signaling Peptides and Proteins", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Islets of Langerhans", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Mice", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Mice, Knockout", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Phenotype", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Phosphoproteins", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Receptor, Insulin", 
        "type": "DefinedTerm"
      }
    ], 
    "author": [
      {
        "affiliation": {
          "alternateName": "the Department of Medicine, and the Department of Molecular Biology, Diabetes Unit, Massachusetts General Hospital and Harvard Medical School, 50 Blossom Street, 02114, Boston, Massachusetts, USA", 
          "id": "http://www.grid.ac/institutes/grid.32224.35", 
          "name": [
            "the Department of Medicine, and the Department of Molecular Biology, Diabetes Unit, Massachusetts General Hospital and Harvard Medical School, 50 Blossom Street, 02114, Boston, Massachusetts, USA"
          ], 
          "type": "Organization"
        }, 
        "familyName": "Avruch", 
        "givenName": "Joseph", 
        "id": "sg:person.01074100404.77", 
        "sameAs": [
          "https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01074100404.77"
        ], 
        "type": "Person"
      }
    ], 
    "citation": [
      {
        "id": "sg:pub.10.1038/372182a0", 
        "sameAs": [
          "https://app.dimensions.ai/details/publication/pub.1046415369", 
          "https://doi.org/10.1038/372182a0"
        ], 
        "type": "CreativeWork"
      }, 
      {
        "id": "sg:pub.10.1038/36116", 
        "sameAs": [
          "https://app.dimensions.ai/details/publication/pub.1019591506", 
          "https://doi.org/10.1038/36116"
        ], 
        "type": "CreativeWork"
      }, 
      {
        "id": "sg:pub.10.1038/372186a0", 
        "sameAs": [
          "https://app.dimensions.ai/details/publication/pub.1049271444", 
          "https://doi.org/10.1038/372186a0"
        ], 
        "type": "CreativeWork"
      }
    ], 
    "datePublished": "1998-02", 
    "datePublishedReg": "1998-02-01", 
    "description": "A hallmark of human type 2 diabetes is hyperglycaemia \u2014 an excess of glucose in the bloodstream. Normally, the pancreatic \u03b2-cell compensate for this by secreting more insulin, but this fail-safe mechanism seems to malfunction in patients with the condition. Now, by generating mice that lack the insulin-receptor substrate-2 (IRS-2) gene, one group has shown that IRS-2 may be responsible for both increased insulin resistance and reduced insulin compenation. The knockout mice develop a syndrome that closely resembles human type 2 diabetes and, importantly, they have fewer \u03b2-cells than wild-type mice.", 
    "genre": "article", 
    "id": "sg:pub.10.1038/35998", 
    "isAccessibleForFree": false, 
    "isPartOf": [
      {
        "id": "sg:journal.1018957", 
        "issn": [
          "0028-0836", 
          "1476-4687"
        ], 
        "name": "Nature", 
        "publisher": "Springer Nature", 
        "type": "Periodical"
      }, 
      {
        "issueNumber": "6670", 
        "type": "PublicationIssue"
      }, 
      {
        "type": "PublicationVolume", 
        "volumeNumber": "391"
      }
    ], 
    "keywords": [
      "human type 2 diabetes", 
      "type 2 diabetes", 
      "insulin receptor substrate-2 (IRS-2) gene", 
      "wild-type mice", 
      "\u03b2-cell failure", 
      "insulin resistance", 
      "more insulin", 
      "knockout mice", 
      "\u03b2-cells", 
      "mice", 
      "IRS-2", 
      "diabetes", 
      "excess of glucose", 
      "hyperglycaemia", 
      "patients", 
      "syndrome", 
      "insulin", 
      "fail-safe mechanism", 
      "bloodstream", 
      "hallmark", 
      "glucose", 
      "group", 
      "failure", 
      "malfunction", 
      "genes", 
      "resistance", 
      "mechanism", 
      "excess", 
      "conditions", 
      "compensates", 
      "signals"
    ], 
    "name": "A signal for \u03b2-cell failure", 
    "pagination": "846-847", 
    "productId": [
      {
        "name": "dimensions_id", 
        "type": "PropertyValue", 
        "value": [
          "pub.1027954810"
        ]
      }, 
      {
        "name": "doi", 
        "type": "PropertyValue", 
        "value": [
          "10.1038/35998"
        ]
      }, 
      {
        "name": "pubmed_id", 
        "type": "PropertyValue", 
        "value": [
          "9495335"
        ]
      }
    ], 
    "sameAs": [
      "https://doi.org/10.1038/35998", 
      "https://app.dimensions.ai/details/publication/pub.1027954810"
    ], 
    "sdDataset": "articles", 
    "sdDatePublished": "2022-10-01T06:29", 
    "sdLicense": "https://scigraph.springernature.com/explorer/license/", 
    "sdPublisher": {
      "name": "Springer Nature - SN SciGraph project", 
      "type": "Organization"
    }, 
    "sdSource": "s3://com-springernature-scigraph/baseset/20221001/entities/gbq_results/article/article_268.jsonl", 
    "type": "ScholarlyArticle", 
    "url": "https://doi.org/10.1038/35998"
  }
]
 

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.10.1038/35998'

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

curl -H 'Accept: application/n-triples' 'https://scigraph.springernature.com/pub.10.1038/35998'

Turtle is a human-readable linked data format.

curl -H 'Accept: text/turtle' 'https://scigraph.springernature.com/pub.10.1038/35998'

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

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1038/35998'


 

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

164 TRIPLES      21 PREDICATES      75 URIs      62 LITERALS      20 BLANK NODES

Subject Predicate Object
1 sg:pub.10.1038/35998 schema:about N38458a236e4949968941de0bebc7df30
2 N3a6472eab8d04112ba89dec6e31e357c
3 N431f7cfa56034ecb862f31ac535f8f97
4 N57adb00167ab4b8696b8d6de1b0751b4
5 N596878dca743411bb43b0dbabb2feb6d
6 N78c2bd31cc8c4165a45c3ca89f4d2ee5
7 N819663524e434d01b7a0961179d26d20
8 N90ca7d43d89b40968dd37e3b0fe1e873
9 Nb6c0f1f9c3a141ccb1629096d78c49ce
10 Nc50670d484f84844832bbf3358e263bb
11 Nc661f390d97b4497b22cfd8e5ade2124
12 Nd480eee62df24a369a2805f9c6aec5fc
13 Nd51ad9beb1204fcdb4dc0d0f9062c11c
14 anzsrc-for:06
15 anzsrc-for:0601
16 anzsrc-for:11
17 anzsrc-for:1103
18 schema:author N64093a66100b40aea7730116e58f1fb0
19 schema:citation sg:pub.10.1038/36116
20 sg:pub.10.1038/372182a0
21 sg:pub.10.1038/372186a0
22 schema:datePublished 1998-02
23 schema:datePublishedReg 1998-02-01
24 schema:description A hallmark of human type 2 diabetes is hyperglycaemia — an excess of glucose in the bloodstream. Normally, the pancreatic β-cell compensate for this by secreting more insulin, but this fail-safe mechanism seems to malfunction in patients with the condition. Now, by generating mice that lack the insulin-receptor substrate-2 (IRS-2) gene, one group has shown that IRS-2 may be responsible for both increased insulin resistance and reduced insulin compenation. The knockout mice develop a syndrome that closely resembles human type 2 diabetes and, importantly, they have fewer β-cells than wild-type mice.
25 schema:genre article
26 schema:isAccessibleForFree false
27 schema:isPartOf N4a630fc031d7417da33d38c47b5a4219
28 N8f66a4c18fd5473eb76bd6e26a15fea7
29 sg:journal.1018957
30 schema:keywords IRS-2
31 bloodstream
32 compensates
33 conditions
34 diabetes
35 excess
36 excess of glucose
37 fail-safe mechanism
38 failure
39 genes
40 glucose
41 group
42 hallmark
43 human type 2 diabetes
44 hyperglycaemia
45 insulin
46 insulin receptor substrate-2 (IRS-2) gene
47 insulin resistance
48 knockout mice
49 malfunction
50 mechanism
51 mice
52 more insulin
53 patients
54 resistance
55 signals
56 syndrome
57 type 2 diabetes
58 wild-type mice
59 β-cell failure
60 β-cells
61 schema:name A signal for β-cell failure
62 schema:pagination 846-847
63 schema:productId N33d4c3e1c3ff46ebb453ef0868c66d36
64 Ne6d5767ded674faaa34e9438181b98dd
65 Nf21194a787f9424c8ccb19bae997f483
66 schema:sameAs https://app.dimensions.ai/details/publication/pub.1027954810
67 https://doi.org/10.1038/35998
68 schema:sdDatePublished 2022-10-01T06:29
69 schema:sdLicense https://scigraph.springernature.com/explorer/license/
70 schema:sdPublisher N3dfb1dc9e1354203bac4239f749f0fef
71 schema:url https://doi.org/10.1038/35998
72 sgo:license sg:explorer/license/
73 sgo:sdDataset articles
74 rdf:type schema:ScholarlyArticle
75 N33d4c3e1c3ff46ebb453ef0868c66d36 schema:name pubmed_id
76 schema:value 9495335
77 rdf:type schema:PropertyValue
78 N38458a236e4949968941de0bebc7df30 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
79 schema:name Disease Models, Animal
80 rdf:type schema:DefinedTerm
81 N3a6472eab8d04112ba89dec6e31e357c schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
82 schema:name Humans
83 rdf:type schema:DefinedTerm
84 N3dfb1dc9e1354203bac4239f749f0fef schema:name Springer Nature - SN SciGraph project
85 rdf:type schema:Organization
86 N431f7cfa56034ecb862f31ac535f8f97 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
87 schema:name Insulin Resistance
88 rdf:type schema:DefinedTerm
89 N4a630fc031d7417da33d38c47b5a4219 schema:volumeNumber 391
90 rdf:type schema:PublicationVolume
91 N57adb00167ab4b8696b8d6de1b0751b4 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
92 schema:name Phenotype
93 rdf:type schema:DefinedTerm
94 N596878dca743411bb43b0dbabb2feb6d schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
95 schema:name Intracellular Signaling Peptides and Proteins
96 rdf:type schema:DefinedTerm
97 N64093a66100b40aea7730116e58f1fb0 rdf:first sg:person.01074100404.77
98 rdf:rest rdf:nil
99 N78c2bd31cc8c4165a45c3ca89f4d2ee5 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
100 schema:name Insulin Receptor Substrate Proteins
101 rdf:type schema:DefinedTerm
102 N819663524e434d01b7a0961179d26d20 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
103 schema:name Animals
104 rdf:type schema:DefinedTerm
105 N8f66a4c18fd5473eb76bd6e26a15fea7 schema:issueNumber 6670
106 rdf:type schema:PublicationIssue
107 N90ca7d43d89b40968dd37e3b0fe1e873 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
108 schema:name Mice, Knockout
109 rdf:type schema:DefinedTerm
110 Nb6c0f1f9c3a141ccb1629096d78c49ce schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
111 schema:name Mice
112 rdf:type schema:DefinedTerm
113 Nc50670d484f84844832bbf3358e263bb schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
114 schema:name Islets of Langerhans
115 rdf:type schema:DefinedTerm
116 Nc661f390d97b4497b22cfd8e5ade2124 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
117 schema:name Phosphoproteins
118 rdf:type schema:DefinedTerm
119 Nd480eee62df24a369a2805f9c6aec5fc schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
120 schema:name Diabetes Mellitus, Type 2
121 rdf:type schema:DefinedTerm
122 Nd51ad9beb1204fcdb4dc0d0f9062c11c schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
123 schema:name Receptor, Insulin
124 rdf:type schema:DefinedTerm
125 Ne6d5767ded674faaa34e9438181b98dd schema:name dimensions_id
126 schema:value pub.1027954810
127 rdf:type schema:PropertyValue
128 Nf21194a787f9424c8ccb19bae997f483 schema:name doi
129 schema:value 10.1038/35998
130 rdf:type schema:PropertyValue
131 anzsrc-for:06 schema:inDefinedTermSet anzsrc-for:
132 schema:name Biological Sciences
133 rdf:type schema:DefinedTerm
134 anzsrc-for:0601 schema:inDefinedTermSet anzsrc-for:
135 schema:name Biochemistry and Cell Biology
136 rdf:type schema:DefinedTerm
137 anzsrc-for:11 schema:inDefinedTermSet anzsrc-for:
138 schema:name Medical and Health Sciences
139 rdf:type schema:DefinedTerm
140 anzsrc-for:1103 schema:inDefinedTermSet anzsrc-for:
141 schema:name Clinical Sciences
142 rdf:type schema:DefinedTerm
143 sg:journal.1018957 schema:issn 0028-0836
144 1476-4687
145 schema:name Nature
146 schema:publisher Springer Nature
147 rdf:type schema:Periodical
148 sg:person.01074100404.77 schema:affiliation grid-institutes:grid.32224.35
149 schema:familyName Avruch
150 schema:givenName Joseph
151 schema:sameAs https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01074100404.77
152 rdf:type schema:Person
153 sg:pub.10.1038/36116 schema:sameAs https://app.dimensions.ai/details/publication/pub.1019591506
154 https://doi.org/10.1038/36116
155 rdf:type schema:CreativeWork
156 sg:pub.10.1038/372182a0 schema:sameAs https://app.dimensions.ai/details/publication/pub.1046415369
157 https://doi.org/10.1038/372182a0
158 rdf:type schema:CreativeWork
159 sg:pub.10.1038/372186a0 schema:sameAs https://app.dimensions.ai/details/publication/pub.1049271444
160 https://doi.org/10.1038/372186a0
161 rdf:type schema:CreativeWork
162 grid-institutes:grid.32224.35 schema:alternateName the Department of Medicine, and the Department of Molecular Biology, Diabetes Unit, Massachusetts General Hospital and Harvard Medical School, 50 Blossom Street, 02114, Boston, Massachusetts, USA
163 schema:name the Department of Medicine, and the Department of Molecular Biology, Diabetes Unit, Massachusetts General Hospital and Harvard Medical School, 50 Blossom Street, 02114, Boston, Massachusetts, USA
164 rdf:type schema:Organization
 




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


...