Evidence map›Paper›PMID 23143302›Full record

ArticleThe Journal of clinical investigation2012

Cancer susceptibility and embryonic lethality in Mob1a/1b double-mutant mice.

Miki Nishio, Koichi Hamada, Kohichi Kawahara, Masato Sasaki, Fumihito Noguchi, Shuhei Chiba, Kensaku Mizuno, Satoshi O Suzuki, Youyi Dong, Masaaki Tokuda and 15 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

87 citing papers in PubMed, 153 citations in OpenAlex.

  1. Article
  2. Article
  3. NF2 is Essential for Human Endoderm Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  4. MOB1 deletion in murine mature adipocytes ameliorates obesity and diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Review
  6. Article
  7. HPV18 E7 inhibits LATS1 kinase and activates YAP1 by degrading PTPN14.bioRxiv : the preprint server for biology · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Hippo-TAZ signaling is the master regulator of the onset of triple-negative basal-like breast cancers.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

27 more citing papers are in PubMed but not listed here.

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

25 authors at 8 institutions in 3 countries.

Miki NishioDivision of Cancer Genetics, Medical Institute of Bioregulation, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Koichi Hamada
Kohichi Kawahara
Masato Sasaki
Fumihito Noguchi
Shuhei Chiba
Kensaku Mizuno
Satoshi O Suzuki
Youyi Dong
Masaaki Tokuda
Takumi Morikawa
Hiroki Hikasa
Jonathan Eggenschwiler
Norikazu Yabuta
Hiroshi Nojima
Kentaro Nakagawa
Yutaka Hata
Hiroshi Nishina
Koshi Mimori
Masaki Mori
Takehiko Sasaki
Tak W Mak
Toru Nakano
Satoshi Itami
Akira Suzuki
Kyushu University · JPOsaka University · JPTokyo Medical and Dental University · JPAkita University · JPKagawa University · JPTohoku University · JPHealth Net · USPrinceton University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mps one binder 1a (MOB1A) and MOB1B are key components of the Hippo signaling pathway and are mutated or inactivated in many human cancers. Here we show that intact Mob1a or Mob1b is essential for murine embryogenesis and that loss of the remaining WT Mob1 allele in Mob1a(Δ/Δ)1b(tr/+) or Mob1a(Δ/+)1b(tr/tr) mice results in tumor development. Because most of these cancers resembled trichilemmal carcinomas, we generated double-mutant mice bearing tamoxifen-inducible, keratinocyte-specific homozygous-null mutations of Mob1a and Mob1b (kDKO mice). kDKO mice showed hyperplastic keratinocyte progenitors and defective keratinocyte terminal differentiation and soon died of malnutrition. kDKO keratinocytes exhibited hyperproliferation, apoptotic resistance, impaired contact inhibition, enhanced progenitor self renewal, and increased centrosomes. Examination of Hippo pathway signaling in kDKO keratinocytes revealed that loss of Mob1a/b altered the activities of the downstream Hippo mediators LATS and YAP1. Similarly, YAP1 was activated in some human trichilemmal carcinomas, and some of these also exhibited MOB1A/1B inactivation. Our results clearly demonstrate that MOB1A and MOB1B have overlapping functions in skin homeostasis, and exert their roles as tumor suppressors by regulating downstream elements of the Hippo pathway.

Indexed as

Genes, LethalAbnormalities, MultipleAdaptor Proteins, Signal TransducingAnimalsCarcinomaCell DifferentiationCells, CulturedCell Transformation, NeoplasticEmbryo Culture TechniquesEmbryo, MammalianFemaleGenetic Association StudiesGenetic Predisposition to DiseaseHomeostasisHomozygoteHumansAdaptor Proteins, Signal TransducingIntracellular Signaling Peptides and ProteinsLats1 protein, mouseLATS2 protein, mouseMob1b protein, mouseMOB1 protein, mousePhosphoproteinsProtein KinasesProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID23143302
PMCPMC3533542
OpenAlexW2171141151

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.