Evidence map›Paper›PMID 19293151›Full record

ArticleThe Journal of biological chemistry2009

Identification of Flightless-I as a substrate of the cytokine-independent survival kinase CISK.

Jun Xu, Lan Liao, Jun Qin, Jianming Xu, Dan Liu, Zhou Songyang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Contributions of SGK3 to transporter-related diseases.Frontiers in cell and developmental biology · 2022
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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

6 authors at 2 institutions in 1 country.

Jun XuVerna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas, USA.
Lan Liao
Jun Qin
Jianming Xu
Dan Liu
Zhou Songyang
Baylor College of Medicine · USMars (United States) · US

Funding

Role of AIB3 in Mammary Gland and Breast CancerR01CA119689 · NCI · BAYLOR COLLEGE OF MEDICINE · PI XU, JIANMING · 2005 to 2009
$1.4M
REGULATION OF CELL SURVIVAL BY PROTEIN KINASE CISKR01GM069572 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI SONGYANG, ZHOU · 2004 to 2007
$1.4M
BIOCHEMICAL GENETIC STUDIES OF CELL SURVIVAL PATHWAYSR01CA084208 · NCI · BAYLOR COLLEGE OF MEDICINE · PI SONGYANG, ZHOU · 2001 to 2005
$1.1M
NCI NIH HHS CA119689NCI NIH HHS CA84208NCI NIH HHS R01 CA119689NIGMS NIH HHS GM069572
6 · The paper itself

Abstract

Phosphatidylinositol (PI) 3-kinase mediates multiple pathways that regulate many aspects of the cell including metabolism, survival, migration, and proliferation. Both Akt and cytokine-independent survival kinase (CISK)/SGK3 are known AGC family protein kinases that function downstream of PI 3-kinase. Although the Akt signaling pathway has been studied extensively, the specific signaling cascades that are modulated by CISK remain to be elucidated. To understand CISK function, we affinity-purified the CISK protein complex and identified Flightless-I (FLII) as a novel downstream target of CISK. Here we show that FLII is an in vivo substrate of CISK that functions downstream of PI 3-kinase. CISK can associate with FLII and phosphorylate FLII at residues Ser(436) and Thr(818). FLII has been shown to act as a co-activator for nuclear hormone receptors such as estrogen receptor (ER). We demonstrate here that CISK can enhance ER transcription, which is dependent on its kinase activity, and mutation of CISK phosphorylation sites on FLII attenuates its activity as an ER co-activator. Furthermore, FLII knockdown by RNA interference renders 32D cells more sensitive to interleukin-3 withdrawal-induced apoptosis, suggesting that FLII itself is also a survival factor. These findings support the model that CISK phosphorylates FLII and activates nuclear receptor transcription and suggest a new cell survival signaling pathway mediated by PI 3-kinase and CISK.

Indexed as

AnimalsCarrier ProteinsCell LineCell SurvivalCytoskeletal ProteinsHumansInterleukin-3MiceMicrofilament ProteinsPhosphorylationPhosphoserinePhosphothreonineProtein BindingProtein Serine-Threonine KinasesReceptors, Cytoplasmic and NuclearReceptors, EstrogenCarrier ProteinsCytoskeletal ProteinsFLII protein, humanFlII protein, mouseInterleukin-3Microfilament ProteinsPhosphoserinePhosphothreonineProtein Serine-Threonine KinasesReceptors, Cytoplasmic and NuclearReceptors, EstrogenSerum-Glucocorticoid Regulated KinasesSGK3 protein, humanSgk3 protein, mouseTrans-Activators

Identifiers

PMID19293151
PMCPMC2682886
OpenAlexW2062022363

What OpenQuestion holds

Textmetadata
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.