ArticleMolecular biology of the cell2003
Hic-5 communicates between focal adhesions and the nucleus through oxidant-sensitive nuclear export signal.
Article in Molecular biology of the cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 95 citations in OpenAlex.
- Co-Optimization of in Vitro Biofunctionality and Electrochemical Passivity in Self-Doped TiOACS omega · 2026Article
- Cancer-associated fibroblasts in carcinogenesis.Journal of translational medicine · 2025Review
- A comparative analysis of paxillin and Hic-5 proximity interactomes.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Mitochondrial Reactive Oxygen Species (mROS) Generation and Cancer:International journal of nanomedicine · 2025Review
- Knockdown of mechanosensitive adaptor Hic-5 ameliorates post-traumatic osteoarthritis in rats through repression of MMP-13.Scientific reports · 2023Article
- Physiological and pathological roles of Hic‑5 in several organs (Review).International journal of molecular medicine · 2022Review
- FAK regulates IL-33 expression by controlling chromatin accessibility at c-Jun motifs.Scientific reports · 2021Article
- Paxillin family of focal adhesion adaptor proteins and regulation of cancer cell invasion.International review of cell and molecular biology · 2020Article
- HIC-5 in cancer-associated fibroblasts contributes to esophageal squamous cell carcinoma progression.Cell death & disease · 2019Article
- Regulation of mitochondrial ROS production by HIC-5: a common feature of oncogene-induced senescence and tumor invasiveness?The FEBS journal · 2019Article
- A mitochondrial ROS pathway controls matrix metalloproteinase 9 levels and invasive properties in RAS-activated cancer cells.The FEBS journal · 2019Article
- The impact of stromal Hic-5 on the tumorigenesis of colorectal cancer through lysyl oxidase induction and stromal remodeling.Oncogene · 2018Article
- Signaling Mechanisms of Myofibroblastic Activation: Outside-in and Inside-Out.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018Review
- Hic-5 mediates the initiation of endothelial sprouting by regulating a key surface metalloproteinase.Journal of cell science · 2016Article
- Hydrogen peroxide inducible clone-5 mediates reactive oxygen species signaling for hepatocellular carcinoma progression.Oncotarget · 2015Article
- Leupaxin is expressed in mammary carcinoma and acts as a transcriptional activator of the estrogen receptor α.International journal of oncology · 2015Article
- Multidimensional analysis of gene expression reveals TGFB1I1-induced EMT contributes to malignant progression of astrocytomas.Oncotarget · 2014Article
- A HIC-5- and KLF4-dependent mechanism transactivates p21(Cip1) in response to anchorage loss.The Journal of biological chemistry · 2012Article
- Hic-5 controls BMP4 responses in prostate cancer cells through interacting with Smads 1, 5 and 8.Oncogene · 2012Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
hic-5 was originally isolated as an H(2)O(2)-inducible cDNA clone whose product was normally found at focal adhesions. In this study, we found that Hic-5 accumulated in the nucleus in response to oxidants such as H(2)O(2). Other focal adhesion proteins including paxillin, the most homologous to Hic-5, remained in the cytoplasm. Mutation analyses revealed that the C- and N-terminal halves of Hic-5 contributed to its nuclear localization in a positive and negative manner, respectively. After the finding that leptomycin B (LMB), an inhibitor of nuclear export signal (NES), caused Hic-5 to be retained in the nucleus, Hic-5 was demonstrated to harbor NES in the N-terminal, which was sensitive to oxidants, thereby regulating the nuclear accumulation of Hic-5. NES consisted of a leucine-rich stretch and two cysteines with a limited similarity to Yap/Pap-type NES. In the nucleus, Hic-5 was suggested to participate in the gene expression of c-fos. Using dominant negative mutants, we found that Hic-5 was actually involved in endogenous c-fos gene expression upon H(2)O(2) treatment. Hic-5 was thus proposed as a focal adhesion protein with the novel aspect of shuttling between focal adhesions and the nucleus through an oxidant-sensitive NES, mediating the redox signaling directly to the nucleus.
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