Evidence map›Paper›PMID 22038529›Full record

ReviewImmunologic research2011

RIP1-mediated regulation of lymphocyte survival and death responses.

Jianke Zhang, Haibing Zhang, Jinghe Li, Stephen Rosenberg, Emily C Zhang, Xiaohui Zhou, Fengsong Qin, Mathew Farabaugh

Abstract readReview
In one paragraph

Review in Immunologic research, 2011. 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
0.9field-weighted citation impact, top 26% 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, 35 citations in OpenAlex.

  1. Article
  2. Functions of the RIP kinase family members in the skin.Cellular and molecular life sciences : CMLS · 2023
    Review
  3. Article
  4. Article
  5. Programmed Necrosis in Host Defense.Current topics in microbiology and immunology · 2023
    Article
  6. Review
  7. Article
  8. Induction and Detection of Necroptotic Cell Death in Mammalian Cell Culture.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

8 authors at 3 institutions in 2 countries.

Jianke ZhangDepartment of Microbiology and Immunology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA. jzhang@mail.jci.tju.edu
Haibing Zhang
Jinghe Li
Stephen Rosenberg
Emily C Zhang
Xiaohui Zhou
Fengsong Qin
Mathew Farabaugh
Thomas Jefferson University · USJilin University · CNShanghai Public Health Clinical Center · CN

Funding

Impact of Cyclin D1 Isoforms in Breast CancerR01CA137494 · NCI · THOMAS JEFFERSON UNIVERSITY · PI KNUDSEN, ERIK, PESTELL, RICHARD G · 2010 to 2014
$1.5M
Apoptosis and Proliferation Signaling Mediated by FADDR01CA095454 · NCI · THOMAS JEFFERSON UNIVERSITY · PI ZHANG, JIANKE · 2002 to 2006
$1.4M
Nit1-mediated signaling in T cellsR21AI083915 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI ZHANG, JIANKE · 2009 to 2010
$425k
The Function of cFLIP in B LymphocytesR03AI076788 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI ZHANG, JIANKE · 2008 to 2009
$155k
NCI NIH HHS CA137494NCI NIH HHS CA95454NCI NIH HHS R01 CA095454NCI NIH HHS R01 CA137494NIAID NIH HHS AI076788NIAID NIH HHS AI083915NIAID NIH HHS R03 AI076788NIAID NIH HHS R21 AI083915
6 · The paper itself

Abstract

RIP1 is an adaptor serine/threonine kinase associated with the signaling complex of death receptors (DRs) including Fas, TNFR1, and TRAIL-Rs which can initiate apoptosis. While DRs are dispensable throughout development, RIP1 deletion results in perinatal lethality. The developmental defect caused by absence of RIP1 remains unexplained. In previous studies, RIP1-deficient hematopoietic progenitors failed to reconstitute the T cell compartment and our recent data indicate a new role for RIP1 in TCR-induced activation of the pro-survival NF-κB pathway. Here, we show that RIP1 is also critical for B cell development. In addition, RIP1(-/-) B cells stimulated through LPS/TLR4 are impaired in NF-κB activation but have no major defect in the Akt pathway. Recently, RIP1 has also emerged as a critical player in necrosis-like death, necroptosis, in various cell lines. We have demonstrated that RIP1 deficiency can reverse the embryonic and T cell proliferation defects in mice lacking FADD, a caspase adaptor protein, which indicates a potential role for RIP1 in mediating in vivo necroptosis. We provide an overview and discussion of the accumulating data revealing insights into the diverse functions of RIP1 in survival and death signaling in lymphocytes.

Indexed as

AnimalsCell SurvivalFas-Associated Death Domain ProteinGTPase-Activating ProteinsHumansLymphocytesMiceMice, KnockoutNecrosisNF-kappa BProto-Oncogene Proteins c-aktSignal TransductionFadd protein, mouseFas-Associated Death Domain ProteinGTPase-Activating ProteinsNF-kappa BProto-Oncogene Proteins c-aktRalbp1 protein, mouse

Identifiers

PMID22038529
PMCPMC3244575
OpenAlexW2118436468

What OpenQuestion holds

Textmetadata
LicenceTDM
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.