Evidence map›Paper›PMID 23695829›Full record

ReviewChannels (Austin, Tex.)

Emerging roles of Orai3 in pathophysiology.

Rajender K Motiani, Judith A Stolwijk, Rachel L Newton, Xuexin Zhang, Mohamed Trebak

Open access · goldAbstract readReview
In one paragraph

Review in Channels (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Store-operated calcium entry-based targets for novel cancer therapeutic development.The Journal of pharmacology and experimental therapeutics · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Arachidonic acid-induced CaCancer cell international · 2018
    Article
  15. ORAI Calcium Channels.Physiology (Bethesda, Md.) · 2017
    Review
  16. Article
  17. Article
  18. The role of STIM and ORAI proteins in phagocytic immune cells.American journal of physiology. Cell physiology · 2016
    Review
  19. Review
  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 3 institutions in 2 countries.

Rajender K MotianiNanobioscience Constellation; College of Nanoscale Science and Engineering (CNSE); University at Albany; State University of New York; Albany, NY USA; DST-INSPIRE Faculty; Institute of Genomics and Integrative Biology (IGIB); New Delhi, India.
Judith A StolwijkNanobioscience Constellation; College of Nanoscale Science and Engineering (CNSE); University at Albany; State University of New York; Albany, NY USA.
Rachel L NewtonNanobioscience Constellation; College of Nanoscale Science and Engineering (CNSE); University at Albany; State University of New York; Albany, NY USA.
Xuexin ZhangNanobioscience Constellation; College of Nanoscale Science and Engineering (CNSE); University at Albany; State University of New York; Albany, NY USA.
Mohamed TrebakNanobioscience Constellation; College of Nanoscale Science and Engineering (CNSE); University at Albany; State University of New York; Albany, NY USA.
State University of New York · USAlbany Research Institute · USInstitute of Genomics and Integrative Biology · IN

Funding

Receptor-regulated Ca2+ Entry Pathways in Smooth MuscleR01HL097111 · NHLBI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI TREBAK, MOHAMED · 2010 to 2019
$3.7M
NHLBI NIH HHS HL097111NHLBI NIH HHS R01 HL097111
6 · The paper itself

Abstract

Calcium (Ca(2+)) is a ubiquitous second messenger that regulates a plethora of physiological functions. Deregulation of calcium homeostasis has been reported in a wide variety of pathological conditions including cardiovascular disorders, cancer and neurodegenerative diseases. One of the most ubiquitous pathways involved in regulated Ca(2+) influx into cells is the store-operated Ca(2+) entry (SOCE) pathway. In 2006, Orai1 was identified as the channel protein that mediates SOCE in immune cells. Orai1 has two mammalian homologs, Orai2 and Orai3. Although Orai1 has been the most widely studied Orai isoform, Orai3 has recently received significant attention. Under native conditions, Orai3 was demonstrated to be an important component of store-independent arachidonate-regulated Ca(2+) (ARC) entry in HEK293 cells, and more recently of a store-independent leukotrieneC4-regulated Ca(2+) (LRC) entry pathway in vascular smooth muscle cells. Recent studies have shown upregulation of Orai3 in estrogen receptor-expressing breast cancers and a critical role for Orai3 in breast cancer development in immune-compromised mice. Orai3 upregulation was also shown to contribute to vascular smooth muscle remodeling and neointimal hyperplasia caused by vascular injury. Furthermore, Orai3 has been shown to contribute to proliferation of effector T-lymphocytes under oxidative stress. In this review, we will discuss the role of Orai3 in reported pathophysiological conditions and will contribute ideas on the potential role of Orai3 in native Ca(2+) signaling pathways and human disease.

Indexed as

AnimalsBreast NeoplasmsCalciumCalcium ChannelsCalcium SignalingHumansLeukemiaMuscle, Smooth, VascularMyocytes, Smooth MuscleOxidative StressCalciumCalcium ChannelsOrai3 protein, humancancerdiseaseOrai3STIM1store-operated channels

Identifiers

PMID23695829
PMCPMC3913762
OpenAlexW2035521053

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.