Evidence map›Paper›PMID 21993393›Full record

ArticleCell death & disease2011

βA3/A1-Crystallin controls anoikis-mediated cell death in astrocytes by modulating PI3K/AKT/mTOR and ERK survival pathways through the PKD/Bit1-signaling axis.

B Ma, T Sen, L Asnaghi, M Valapala, F Yang, S Hose, D S McLeod, Y Lu, C Eberhart, J S Zigler and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Involvement of Anoikis in Dissociated Optic Nerve Fiber Layer Appearance.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Bit1-a potential positive regulator of epithelial-mesenchymal transition in lens epithelial cells.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2016
    Article
  16. Review
  17. Article
  18. Article
  19. βA3/A1-crystallin: more than a lens protein.Progress in retinal and eye research · 2015
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

B MaThe Wilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
T Sen
L Asnaghi
M Valapala
F Yang
S Hose
D S McLeod
Y Lu
C Eberhart
J S Zigler
D Sinha
Johns Hopkins Medicine · USJohns Hopkins University · USEye & ENT Hospital of Fudan University · CN

Funding

Wilmer Core Grant for Vision ResearchP30EY001765 · NEI · JOHNS HOPKINS UNIVERSITY · PI Jiang Qian · 1985 to 2026
$22.1M
A novel bA3/A1-crystallin gene mutation results in persistent fetal vasculatureR01EY019037 · NEI · JOHNS HOPKINS UNIVERSITY · PI SINHA, DEBASISH · 2008 to 2015
$4.1M
A CRYSTALLIN MUTATION WITH ABNORMAL ASTROCYTES AND RETINAL VESSELSR01EY018636 · NEI · JOHNS HOPKINS UNIVERSITY · PI SINHA, DEBASISH · 2009 to 2010
$820k
NEI NIH HHS EY01765NEI NIH HHS EY018636NEI NIH HHS EY019037NEI NIH HHS EY019037-SNEI NIH HHS P30 EY001765NEI NIH HHS R01 EY018636NEI NIH HHS R01 EY019037
6 · The paper itself

Abstract

During eye development, apoptosis is vital to the maturation of highly specialized structures such as the lens and retina. Several forms of apoptosis have been described, including anoikis, a form of apoptosis triggered by inadequate or inappropriate cell-matrix contacts. The anoikis regulators, Bit1 (Bcl-2 inhibitor of transcription-1) and protein kinase-D (PKD), are expressed in developing lens when the organelles are present in lens fibers, but are downregulated as active denucleation is initiated. We have previously shown that in rats with a spontaneous mutation in the Cryba1 gene, coding for βA3/A1-crystallin, normal denucleation of lens fibers is inhibited. In rats with this mutation (Nuc1), both Bit1 and PKD remain abnormally high in lens fiber cells. To determine whether βA3/A1-crystallin has a role in anoikis, we induced anoikis in vitro and conducted mechanistic studies on astrocytes, cells known to express βA3/A1-crystallin. The expression pattern of Bit1 in retina correlates temporally with the development of astrocytes. Our data also indicate that loss of βA3/A1-crystallin in astrocytes results in a failure of Bit1 to be trafficked to the Golgi, thereby suppressing anoikis. This loss of βA3/A1-crystallin also induces insulin-like growth factor-II, which increases cell survival and growth by modulating the phosphatidylinositol-3-kinase (PI3K)/AKT/mTOR and extracellular signal-regulated kinase pathways. We propose that βA3/A1-crystallin is a novel regulator of both life and death decisions in ocular astrocytes.

Indexed as

AnimalsAnoikisApoptosisAstrocytesCarboxylic Ester HydrolasesCrystallinsExtracellular Signal-Regulated MAP KinasesPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySignal TransductionTOR Serine-Threonine KinasesbetaA3-crystallin, ratCarboxylic Ester HydrolasesCrystallinsExtracellular Signal-Regulated MAP KinasesPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID21993393
PMCPMC3219085
OpenAlexW2087565211

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.