Document Type

Letter to the Editor

Publisher

Higher Education Pres

Faculty

Health, Engineering and Science

School

School of Medical Science

RAS ID

19927

Comments

This article was originally published as: Xing, Y., Chu, Q., Feng, R., Wang, W., Liu, L., & Lu, Z. (2015). hCLP46 increases Smad3 protein stability via inhibiting its ubiquitin-proteasomal degradation. Protein & cell, 6(10), 767-770. Original article available here

Abstract

hCLP46 (human CAP10-like protein 46 kDa) was initially isolated and identified from human acute myeloid leukemia transformed from myelodysplastic syndrome (MDS-AML) CD34+ cells (Teng et al., 2006) and we demonstrated previously that hCLP46 is abnormally expressed in many hematopoietic malignancies (Wang et al., 2010). Studies fromits Drosophila homolog, Rumi, suggested that Notch is a potential target of hCLP46 (Acar et al., 2008). We also found that overexpression of hCLP46 enhances Notch activation and regulates cell proliferation in a cell type-dependent manner (Ma et al., 2011; Chu et al., 2013). However, hCLP46/embryos show more severe phenotypes compared to those displayed by other global regulators of canonical Notch signaling, suggesting that hCLP46 is likely to have additional important targets during mammalian development (Fernandez- Valdivia et al., 2011). Based on the crosstalk between Notch and the transforming growth factor-β (TGF-β) signaling, we proposed that hCLP46 might be involved in TGF-β signal regulation, but the detail mechanism remains unclear.

DOI

10.1007/s13238-015-0174-0

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

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