Evidence map›Paper›PMID 20573984›Full record

ArticleMolecular biology of the cell2010

Regulation of genotoxic stress response by homeodomain-interacting protein kinase 2 through phosphorylation of cyclic AMP response element-binding protein at serine 271.

Kensuke Sakamoto, Bo-Wen Huang, Kenta Iwasaki, Kiros Hailemariam, Jun Ninomiya-Tsuji, Yoshiaki Tsuji

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. What turns CREB on? And off? And why does it matter?Cellular and molecular life sciences : CMLS · 2020
    Review
  5. Review
  6. Article
  7. ER Stress, CREB, and Memory: A Tangled Emerging Link in Disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2019
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

6 authors at 2 institutions in 2 countries.

Kensuke SakamotoDepartment of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, NC 27695, USA.
Bo-Wen Huang
Kenta Iwasaki
Kiros Hailemariam
Jun Ninomiya-Tsuji
Yoshiaki Tsuji
North Carolina State University · USCenter for Food Safety and Applied Nutrition · US

Funding

TRAINING IN BIOCHEMICAL AND ENVIRONMENTAL TOXICOLOGYT32ES007046 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Seth William Kullman · 1985 to 2026
$5.1M
TAK1 signaling network in tissue homeostasisR01GM068812 · NIGMS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI NINOMIYA-TSUJI, JUN · 2004 to 2013
$2.4M
REGULATION OF IRON HOMEOSTASIS IN OXIDATIVE STRESSR01DK060007 · NIDDK · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI TSUJI, YOSHIAKI · 2002 to 2005
$1.2M
NIDDK NIH HHS DK-60007NIDDK NIH HHS DK-60007SNIDDK NIH HHS R01 DK060007NIEHS NIH HHS ES-007046NIEHS NIH HHS T32 ES007046NIGMS NIH HHS GM068812NIGMS NIH HHS R01 GM068812
6 · The paper itself

Abstract

CREB (cyclic AMP response element-binding protein) is a stimulus-induced transcription factor that plays pivotal roles in cell survival and proliferation. The transactivation function of CREB is primarily regulated through Ser-133 phosphorylation by cAMP-dependent protein kinase A (PKA) and related kinases. Here we found that homeodomain-interacting protein kinase 2 (HIPK2), a DNA-damage responsive nuclear kinase, is a new CREB kinase for phosphorylation at Ser-271 but not Ser-133, and activates CREB transactivation function including brain-derived neurotrophic factor (BDNF) mRNA expression. Ser-271 to Glu-271 substitution potentiated the CREB transactivation function. ChIP assays in SH-SY5Y neuroblastoma cells demonstrated that CREB Ser-271 phosphorylation by HIPK2 increased recruitment of a transcriptional coactivator CBP (CREB binding protein) without modulation of CREB binding to the BDNF CRE sequence. HIPK2-/- MEF cells were more susceptible to apoptosis induced by etoposide, a DNA-damaging agent, than HIPK2+/+ cells. Etoposide activated CRE-dependent transcription in HIPK2+/+ MEF cells but not in HIPK2-/- cells. HIPK2 knockdown in SH-SY5Y cells decreased etoposide-induced BDNF mRNA expression. These results demonstrate that HIPK2 is a new CREB kinase that regulates CREB-dependent transcription in genotoxic stress.

Indexed as

DNA DamageAnimalsAntineoplastic Agents, PhytogenicBlotting, WesternBrain-Derived Neurotrophic FactorCarrier ProteinsCell Line, TumorCells, CulturedCREB-Binding ProteinCyclic AMP Response Element-Binding ProteinEmbryo, MammalianEtoposideFibroblastsHEK293 CellsHumansK562 CellsAntineoplastic Agents, PhytogenicBrain-Derived Neurotrophic FactorCarrier ProteinsCREB-Binding ProteinCyclic AMP Response Element-Binding ProteinEtoposideHIPK2 protein, humanProtein Serine-Threonine KinasesSerine

Identifiers

PMID20573984
PMCPMC2921112
OpenAlexW1992486930

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.