Evidence map›Paper›PMID 18565850›Full record

ArticleBlood2008

Defective homing is associated with altered Cdc42 activity in cells from patients with Fanconi anemia group A.

Xiaoling Zhang, Xun Shang, Fukun Guo, Kim Murphy, Michelle Kirby, Patrick Kelly, Lilith Reeves, Franklin O Smith, David A Williams, Yi Zheng and 1 more

Abstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Review
  2. Article
  3. Dynamic Tracking of Native Precursors in Adult Mice.bioRxiv : the preprint server for biology · 2024
    Article
  4. Roles of USP1 in Ewing sarcoma.Genes & cancer · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Genetic correction of hematopoiesis in Fanconi anemia: the case for a non-HSC-autonomous defect.Molecular therapy : the journal of the American Society of Gene Therapy · 2009
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Xiaoling ZhangDivision of Experimental Hematology, Cincinnati Children's Research Foundation and Fanconi Anemia Comprehensive Care Center, Cincinnati Children's Hospital Medical Center, OH 45229, USA.
Xun Shang
Fukun Guo
Kim Murphy
Michelle Kirby
Patrick Kelly
Lilith Reeves
Franklin O Smith
David A Williams
Yi Zheng
Qishen Pang

Funding

VITAMIN K DEFICIENCY IN CHOLESTATIC LIVER DISEASEM01RR008084 · NCRR · CINCINNATI CHILDRENS HOSP MED CTR · PI HEUBI, JAMES E. · 1994 to 2009
$20.6M
Role of FA Proteins in HematopoiesisR01HL076712 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI PANG, QISHEN · 2005 to 2020
$5.0M
Cell Type and Stimulus-Specific Signaling Role of CDC42 in BloodR01HL085362 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2006 to 2010
$2.0M
Novel Molecular and Cellular Therapies in Fanconi AnemiaR01HL081499 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI WILLIAMS, DAVID A · 2006 to 2009
$1.3M
NCRR NIH HHS M01 RR008084NCRR NIH HHS M01 RR 08084NHLBI NIH HHS R01 HL076712NHLBI NIH HHS R01 HL081499NHLBI NIH HHS R01 HL085362
6 · The paper itself

Abstract

Previous studies showed that Fanconi anemia (FA) murine stem cells have defective reconstitution after bone marrow (BM) transplantation. The mechanism underlying this defect is not known. Here, we report defective homing of FA patient BM progenitors transplanted into mouse models. Using cells from patients carrying mutations in FA complementation group A (FA-A), we show that when transplanted into nonobese diabetic/severe combined immunodeficiency (NOD/SCID) recipient mice, FA-A BM cells exhibited impaired homing activity. FA-A cells also showed defects in both cell-cell and cell-matrix adhesion. Complementation of FA-A deficiency by reexpression of FANCA readily restored adhesion of FA-A cells. A significant decrease in the activity of the Rho GTPase Cdc42 was found associated with these defective functions in patient-derived cells, and expression of a constitutively active Cdc42 mutant was able to rescue the adhesion defect of FA-A cells. These results provide the first evidence that FA proteins influence human BM progenitor homing and adhesion via the small GTPase Cdc42-regulated signaling pathway.

Indexed as

AdolescentAdultAnimalsBone Marrow CellsBone Marrow TransplantationCase-Control Studiescdc42 GTP-Binding ProteinCell AdhesionCell MovementChildColony-Forming Units AssayFanconi AnemiaHematopoietic Stem CellsHumansMiceMice, Inbred NODcdc42 GTP-Binding Protein

Identifiers

PMID18565850
PMCPMC2518878

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.