Evidence map›Paper›PMID 18687124›Full record

ArticleMolecular cancer2008

The parafibromin tumor suppressor protein interacts with actin-binding proteins actinin-2 and actinin-3.

Sunita K Agarwal, William F Simonds, Stephen J Marx

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The roles of the tumor suppressor parafibromin in cancer.Frontiers in cell and developmental biology · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. High Expression Levels ofJournal of Cancer · 2019
    Article
  10. Article
  11. Article
  12. The roles of parafibromin expression in ovarian epithelial carcinomas: a marker for differentiation and prognosis and a target for gene therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  13. The clinicopathological significances and biological functions of parafibromin expression in head and neck squamous cell carcinomas.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  14. Article
  15. Article
  16. Clinical and molecular genetics of parathyroid neoplasms.Best practice & research. Clinical endocrinology & metabolism · 2010
    Review
  17. Article
  18. Hyperparathyroid genes: sequences reveal answers and questions.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
    Review
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

3 authors at 1 institution in 1 country.

Sunita K AgarwalNational Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA. sunitaa@mail.nih.gov
William F Simonds
Stephen J Marx
National Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Mechanism of Action of the HRPT2 Tumor Suppressor Gene Product ParafibrominZIADK043320 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SIMONDS, WILLIAM F · 2009 to 2017
$4.0M
Mechanism of Action of the HRPT2 Tumor Suppressor Gene Product ParafibrominZ01DK043320 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SIMONDS, WILLIAM F · 2007 to 2008
$680k
Intramural NIH HHS
6 · The paper itself

Abstract

backgroundGermline and somatic inactivating mutations in the HRPT2 gene occur in the inherited hyperparathyroidism-jaw tumor syndrome, in some cases of parathyroid cancer and in some cases of familial hyperparathyroidism. HRPT2 encodes parafibromin. To identify parafibromin interacting proteins we used the yeast two-hybrid system for screening a heart cDNA library with parafibromin as the bait.

resultsFourteen parafibromin interaction positive preys representing 10 independent clones encoding actinin-2 were isolated. Parafibromin interacted with muscle alpha-actinins (actinin-2 and actinin-3), but not with non-muscle alpha-actinins (actinin-1 and actinin-4). The parafibromin-actinin interaction was verified by yeast two-hybrid, GST pull-down, and co-immunoprecipitation. Yeast two-hybrid analysis revealed that the N-terminal region of parafibromin interacted with actinins. In actin sedimentation assays parafibromin did not dissociate skeletal muscle actinins from actin filaments, but interestingly, parafibromin could also bundle/cross-link actin filaments. Parafibromin was predominantly nuclear in undifferentiated proliferating myoblasts (C2C12 cells), but in differentiated C2C12 myotubes parafibromin co-localized with actinins in the cytoplasmic compartment.

conclusionThese data support a possible contribution of parafibromin outside the nucleus through its interaction with actinins and actin bundling/cross-linking. These data also suggest that actinins (and actin) participate in sequestering parafibromin in the cytoplasmic compartment.

Indexed as

ActininAnimalsCell NucleusCells, CulturedCytoplasmFluorescent Antibody TechniqueGene LibraryHeLa CellsHumansMiceParathyroid NeoplasmsTransfectionTumor Suppressor ProteinsTwo-Hybrid System TechniquesActininACTN2 protein, humanACTN3 protein, humanCDC73 protein, humanTumor Suppressor Proteins

Identifiers

PMID18687124
PMCPMC2519076
OpenAlexW2169913586

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.