ArticleThe Biochemical journal2002
A new c-Jun N-terminal kinase (JNK)-interacting protein, Sab (SH3BP5), associates with mitochondria.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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.
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.
Who cites it
51 citing papers in PubMed.
- Role of lipid-associated fibroblasts and their signature genes FABP4, CD36 and ABCA8 in gastric cancer progression.Oncology letters · 2026Article
- Review
- Targeting of kinases to treat neurodegenerative diseases.Pharmacological reviews · 2026Review
- SH3BP5L triggers the RAB11A-regulated integrin recycling network implicated in breast cancer metastasis.The Journal of clinical investigation · 2026Article
- Jiangzhi Granule Ameliorates JNK-Mediated Mitochondrial Dysfunction to Reduce Lipotoxic Liver Injury in NASH.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Mitochondrial P-JNK target, SAB (SH3BP5), in regulation of cell death.Frontiers in cell and developmental biology · 2024Review
- Selective inhibition of JNK located on mitochondria protects against mitochondrial dysfunction and cell death caused by endoplasmic reticulum stress in mice with LPS‑induced ALI/ARDS.International journal of molecular medicine · 2022Article
- Dusp26 phosphatase regulates mitochondrial respiration and oxidative stress and protects neuronal cell death.Cellular and molecular life sciences : CMLS · 2022Article
- Scoparone Improves Nonalcoholic Steatohepatitis Through Alleviating JNK/Sab Signaling Pathway-Mediated Mitochondrial Dysfunction.Frontiers in pharmacology · 2022Article
- Tankyrase regulates epithelial lumen formation via suppression of Rab11 GEFs.The Journal of cell biology · 2021Article
- Selective inhibition of JNK mitochondrial location is protective against seawater inhalation‑induced ALI/ARDS.Molecular medicine reports · 2021Article
- Mitochondrial Kinases and the Role of Mitochondrial Protein Phosphorylation in Health and Disease.Life (Basel, Switzerland) · 2021Review
- Peroxiredoxin 6 mediates acetaminophen-induced hepatocyte death through JNK activation.Redox biology · 2020Article
- Type 3 Inositol 1,4,5-Trisphosphate Receptor Is Increased and Enhances Malignant Properties in Cholangiocarcinoma.Hepatology (Baltimore, Md.) · 2020Article
- Expression of mitochondrial membrane-linked SAB determines severity of sex-dependent acute liver injury.The Journal of clinical investigation · 2019Article
- Elevated SH3BP5 Correlates with Poor Outcome and Contributes to the Growth of Acute Myeloid Leukemia Cells.Biomolecules · 2019Article
- Phosphoregulation on mitochondria: Integration of cell and organelle responses.CNS neuroscience & therapeutics · 2019Review
- Article
- The Regulation of JNK Signaling Pathways in Cell Death through the Interplay with Mitochondrial SAB and Upstream Post-Translational Effects.International journal of molecular sciences · 2018Review
- Structural determinants of Rab11 activation by the guanine nucleotide exchange factor SH3BP5.Nature communications · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have identified a novel c-Jun N-terminal kinase (JNK)-interacting protein, Sab, by yeast two-hybrid screening. Sab binds to and serves as a substrate for JNK in vitro, and was previously found to interact with the Src homology 3 (SH3) domain of Bruton's tyrosine kinase (Btk). Inspection of the sequence of Sab reveals the presence of two putative mitogen-activated protein kinase interaction motifs (KIMs) similar to that found in the JNK docking domain of the c-Jun transcription factor, and four potential serine-proline JNK phosphorylation sites in the C-terminal half of the molecule. Using deletion and site-directed mutagenesis, we demonstrate that the most N-terminal KIM in Sab is essential for JNK binding, and that, as with c-Jun, physical interaction with JNK is necessary for Sab phosphorylation. Interestingly, confocal immunocytochemistry and cell fractionation studies indicate that Sab is associated with mitochondria, where it co-localizes with a fraction of active JNK. These and previously reported properties of Sab suggest a possible role in targeting JNK to this subcellular compartment and/or mediating cross-talk between the Btk and JNK signal transduction pathways.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.