Evidence map›Paper›PMID 20302626›Full record

ArticleBMC biology2010

ASB9 interacts with ubiquitous mitochondrial creatine kinase and inhibits mitochondrial function.

Sanghoon Kwon, Dongbum Kim, Jae Won Rhee, Jeong-A Park, Dae-Won Kim, Doo-Sik Kim, Younghee Lee, Hyung-Joo Kwon

Open access · goldAbstract read
In one paragraph

Article in BMC biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 61 citations in OpenAlex.

  1. ASB9 promotes ubiquitin-mediated degradation of TNP2 to facilitate histone-to-protamine transition in humans and mice.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  9. Ubiquitous mitochondrial creatine kinase promotes the progression of gastric cancer through a JNK-MAPK/JUN/HK2 axis regulated glycolysis.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023
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  16. Morphine Binds Creatine Kinase B and Inhibits Its Activity.Frontiers in cellular neuroscience · 2018
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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

8 authors at 2 institutions in 1 country.

Sanghoon KwonDepartment of Microbiology, College of Medicine, Hallym University, Gangwon-do, Republic of Korea.
Dongbum Kim
Jae Won Rhee
Jeong-A Park
Dae-Won Kim
Doo-Sik Kim
Younghee Lee
Hyung-Joo Kwon
Hallym University · KRChungbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe ankyrin repeat and suppressor of cytokine signalling (SOCS) box proteins (Asbs) are a large protein family implicated in diverse biological processes including regulation of proliferation and differentiation. The SOCS box of Asb proteins is important in a ubiquitination-mediated proteolysis pathway. Here, we aimed to evaluate expression and function of human Asb-9 (ASB9).

resultsWe found that a variant of ASB9 that lacks the SOCS box (ASB9DeltaSOCS) was naturally detected in human cell lines but not in peripheral blood mononuclear cells or normal hepatocytes. We also identified ubiquitous mitochondrial creatine kinase (uMtCK) as a new target of ASB9 in human embryonic kidney 293 (HEK293) cells. The ankyrin repeat domains of ASB9 can associate with the substrate binding site of uMtCK in a SOCS box-independent manner. The overexpression of ASB9, but not ASB9DeltaSOCS, induces ubiquitination of uMtCK. ASB9 and ASB9DeltaSOCS can interact and colocalise with uMtCK in the mitochondria. However, only expression of ASB9 induced abnormal mitochondrial structure and a decrease of mitochondrial membrane potential. Furthermore, the creatine kinase activities and cell growth were significantly reduced by ASB9 but not by ASB9DeltaSOCS.

conclusionsASB9 interacts with the creatine kinase system and negatively regulates cell growth. The differential expression and function of ASB9 and ASB9DeltaSOCS may be a key factor in the growth of human cell lines and primary cells.

Indexed as

Amino Acid SequenceAnkyrin RepeatBinding SitesCell LineCell ProliferationCells, CulturedCreatine Kinase, Mitochondrial FormHumansMembrane Potential, MitochondrialMitochondriaMolecular Sequence DataProtein BindingReverse Transcriptase Polymerase Chain ReactionSequence Homology, Amino AcidSuppressor of Cytokine Signaling ProteinsUbiquitinationASB9 protein, humanCreatine Kinase, Mitochondrial FormSuppressor of Cytokine Signaling Proteins

Identifiers

PMID20302626
PMCPMC2852384
OpenAlexW2015038226

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.