Evidence map›Paper›PMID 26557810›Full record

ArticleImmune network2015

Engagement of CD99 Reduces AP-1 Activity by Inducing BATF in the Human Multiple Myeloma Cell Line RPMI8226.

Minchan Gil, Hyo-Kyung Pak, Seo-Jeong Park, A-Neum Lee, Young-Soo Park, Hyangsin Lee, Hyunji Lee, Kyung-Eun Kim, Kyung Jin Lee, Dok Hyun Yoon and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Immune network, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

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  10. Chemical Constituents Identified from Fruit Body ofBiomolecules & therapeutics · 2017
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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

12 authors at 4 institutions in 1 country.

Minchan GilCell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Hyo-Kyung PakCell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Seo-Jeong ParkCell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
A-Neum LeeCell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Young-Soo ParkDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Hyangsin LeeCell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Hyunji LeeCell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Kyung-Eun KimSIS Immunology Research Center, Sookmyung Women's University, Seoul 04310, Korea.
Kyung Jin LeeInstitute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Dok Hyun YoonDepartment of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Yoo-Sam ChungDepartment of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Chan-Sik ParkCell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul 05505, Korea. ; Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Ulsan College · KRUniversity of Ulsan · KRAsan Medical Center · KRSookmyung Women's University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD99 signaling is crucial to a diverse range of biological functions including survival and proliferation. CD99 engagement is reported to augment activator protein-1 (AP-1) activity through mitogen-activated protein (MAP) kinase pathways in a T-lymphoblastic lymphoma cell line Jurkat and in breast cancer cell lines. In this study, we report that CD99 differentially regulated AP-1 activity in the human myeloma cell line RPMI8226. CD99 was highly expressed and the CD99 engagement led to activation of the MAP kinases, but suppressed AP-1 activity by inducing the expression of basic leucine zipper transcription factor, ATF-like (BATF), a negative regulator of AP-1 in RPMI8226 cells. By contrast, engagement of CD99 enhanced AP-1 activity and did not change the BATF expression in Jurkat cells. CD99 engagement reduced the proliferation of RPMI8226 cells and expression of cyclin 1 and 3. Overall, these results suggest novel CD99 functions in RPMI8226 cells.

Indexed as

AP-1BATFCD99MAP kinaseProliferation

Identifiers

PMID26557810
PMCPMC4637347
OpenAlexW2145112313

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.