Evidence map›Paper›PMID 21931116›Full record

ArticleBlood2011

The role of Skp2 in hematopoietic stem cell quiescence, pool size, and self-renewal.

Jing Wang, Fei Han, Juan Wu, Szu-Wei Lee, Chia-Hsin Chan, Ching-Yuan Wu, Wei-Lei Yang, Yuan Gao, Xian Zhang, Yun Seong Jeong and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. E3 ubiquitin ligase on the biological properties of hematopoietic stem cell.Journal of molecular medicine (Berlin, Germany) · 2023
    Review
  10. Article
  11. Review
  12. Molecular regulation of hematopoietic stem cell quiescence.Cellular and molecular life sciences : CMLS · 2022
    Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Quiescence Entry, Maintenance, and Exit in Adult Stem Cells.International journal of molecular sciences · 2019
    Review
  19. 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

16 authors at 5 institutions in 3 countries.

Jing WangDepartment of Molecular and Cellular Oncology, M. D. Anderson Cancer Center, The University of Texas, Houston, TX, USA.
Fei Han
Juan Wu
Szu-Wei Lee
Chia-Hsin Chan
Ching-Yuan Wu
Wei-Lei Yang
Yuan Gao
Xian Zhang
Yun Seong Jeong
Asad Moten
Felipe Samaniego
Peng Huang
Quentin Liu
Yi-Xin Zeng
Hui-Kuan Lin
The University of Texas MD Anderson Cancer Center · USSun Yat-sen University · CNChang Gung University · TWPathways Behavioral Services · USSun Yat-sen University Cancer Center · CN

Funding

Targeting Fas Inhibitors in Cancer TherapyR21CA153170 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SAMANIEGO, FELIPE · 2010 to 2011
$373k
NCI NIH HHS R21 CA153170
6 · The paper itself

Abstract

Although the maintenance of HSC quiescence and self-renewal are critical for controlling stem cell pool and transplantation efficiency, the mechanisms by which they are regulated remain largely unknown. Understanding the factors controlling these processes may have important therapeutic potential for BM failure and cancers. Here, we show that Skp2, a component of the Skp2 SCF complex, is an important regulator for HSC quiescence, frequency, and self-renewal capability. Skp2 deficiency displays a marked enhancement of HSC populations through promoting cell cycle entry independently of its role on apoptosis. Surprisingly, Skp2 deficiency in HSCs reduces quiescence and displays increased HSC cycling and proliferation. Importantly, loss of Skp2 not only increases HSC populations and long-term reconstitution ability but also rescues the defect in long-term reconstitution ability of HSCs on PTEN inactivation. Mechanistically, we show that Skp2 deficiency induces Cyclin D1 gene expression, which contributes to an increase in HSC cycling. Finally, we demonstrate that Skp2 deficiency enhances sensitivity of Lin(-) Sca-1(+) c-kit(+) cells and leukemia cells to chemotherapy agents. Our findings show that Skp2 is a novel regulator for HSC quiescence and self-renewal and that targeting Skp2 may have therapeutic implications for BM transplantation and leukemia stem cell treatment.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell DivisionCyclin D1Drug Resistance, NeoplasmHematopoietic Stem CellsHematopoietic Stem Cell TransplantationLeukemiaMiceMice, 129 StrainMice, Inbred C57BLMice, Mutant StrainsPTEN PhosphohydrolaseS-Phase Kinase-Associated ProteinsAntineoplastic AgentsCcnd1 protein, mouseCyclin D1PTEN PhosphohydrolasePten protein, mouseS-Phase Kinase-Associated Proteins

Identifiers

PMID21931116
PMCPMC3217347
OpenAlexW2091039289

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.