Evidence map›Paper›PMID 35626682›Full record

ReviewCells2022

The RAL Enigma: Distinct Roles of RALA and RALB in Cancer.

Dillon S Richardson, Jonathan M Spehar, David T Han, Prathik A Chakravarthy, Steven T Sizemore

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Integrating integrins with the hallmarks of cancer.Matrix biology : journal of the International Society for Matrix Biology · 2024
    Review
  17. Article
  18. Genes · 2023
    Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Dillon S RichardsonThe Ohio State University Comprehensive Cancer Center-James Cancer Hospital and Solove Research Institute, Department of Radiation Oncology, The Ohio State University, Columbus, OH 43210, USA.
Jonathan M SpeharThe Ohio State University Comprehensive Cancer Center-James Cancer Hospital and Solove Research Institute, Department of Radiation Oncology, The Ohio State University, Columbus, OH 43210, USA.
David T HanThe Ohio State University Comprehensive Cancer Center-James Cancer Hospital and Solove Research Institute, Department of Radiation Oncology, The Ohio State University, Columbus, OH 43210, USA.
Prathik A ChakravarthyThe Ohio State University Comprehensive Cancer Center-James Cancer Hospital and Solove Research Institute, Department of Radiation Oncology, The Ohio State University, Columbus, OH 43210, USA.
Steven T SizemoreThe Ohio State University Comprehensive Cancer Center-James Cancer Hospital and Solove Research Institute, Department of Radiation Oncology, The Ohio State University, Columbus, OH 43210, USA.
The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · USThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RALA and RALB are highly homologous small G proteins belonging to the RAS superfamily. Like other small GTPases, the RALs are molecular switches that can be toggled between inactive GDP-bound and active GTP-bound states to regulate diverse and critical cellular functions such as vesicle trafficking, filopodia formation, mitochondrial fission, and cytokinesis. The RAL paralogs are activated and inactivated by a shared set of guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs) and utilize similar sets of downstream effectors. In addition to their important roles in normal cell biology, the RALs are known to be critical mediators of cancer cell survival, invasion, migration, and metastasis. However, despite their substantial similarities, the RALs often display striking functional disparities in cancer. RALA and RALB can have redundant, unique, or even antagonistic functions depending on cancer type. The molecular basis for these discrepancies remains an important unanswered question in the field of cancer biology. In this review we examine the functions of the RAL paralogs in normal cellular physiology and cancer biology with special consideration provided to situations where the roles of RALA and RALB are non-redundant.

Indexed as

Monomeric GTP-Binding ProteinsNeoplasmsCell SurvivalGTPase-Activating ProteinsHumansral GTP-Binding ProteinsGTPase-Activating ProteinsMonomeric GTP-Binding ProteinsRALA protein, humanRalb protein, humanral GTP-Binding ProteinscancerendocytosisexocytosisGTPasesRALRALARALBRALBP1RAS

Identifiers

PMID35626682
PMCPMC9139244
OpenAlexW4280582782

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.