The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
GATA-2 inhibits transforming growth factor-β signaling pathway through interaction with Smad4.
Abstract
GATA-2, a member of zinc finger GATA transcription factor family, plays key role in the hematopoietic stem cells self-renewal and differentiation. The transforming growth factor-β (TGFβ) signaling pathway is a major signaling network that controls cell proliferation, differentiation and tumor suppression. Here we found that GATA-2 negatively regulated TGF-β signaling pathway in Smad4-dependent manner. GATA-2 specifically interacts with Smad4 with its N-terminal while the zinc finger domain of GATA-2 is essential for negative regulation of TGFβ. Although GATA-2 did not affect the phosphorylation of Smad2/3 and the complex Smad2/3/4 formation in response to TGFβ, the DNA binding activity of Smad4 was decreased significantly by GATA-2 overexpression. Overexpression of GATA-2 in K562 cells led to reduced TGFβ-induced erythroid differentiation while knockdown of GATA-2 enhanced TGFβ-induced erythroid differentiation. All these results suggest that GATA-2 is a novel negative regulator of TGFβ signal pathway.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“miR-4732-3p overexpression inhibits SMAD4-mediated transcriptional activity”
From Red Blood Cells as Potential Repositories of MicroRNAs in the Circulatory System (2020) · cites this paper as Dong et al., 2014
Citations
Cites
An atlas of combinatorial transcriptional regulation in mouse and man
Ravasi, T., Suzuki, H., Cannistraci, C. V., Katayama, S., Bajic, V. B., Tan, K., Akalin, A., Schmeier, S., Kanamori-Katayama, M., Bertin, N., et al. (2010) · Cell · doi:10.1016/j.cell.2010.01.044 · Cited by 715
Research works printed but not linked: 32
- Rodrigues, 2012, Int. J. Biochem. Cell Biol., 44, 457, 10.1016/j.biocel.2011.12.004 · DOI
- Vicente, 2012, Crit. Rev. Oncol. Hematol., 82, 1, 10.1016/j.critrevonc.2011.04.007 · DOI
- Heyworth, 1999, Genes Dev., 13, 1847, 10.1101/gad.13.14.1847 · DOI
- Tsai, 1994, Nature, 371, 221, 10.1038/371221a0 · DOI
- Ohneda, 2002, Acta Haematol., 108, 237, 10.1159/000065660 · DOI
- Tsai, 1997, Blood, 89, 3636, 10.1182/blood.V89.10.3636 · DOI
- Kitajima, 2002, EMBO J., 21, 3060, 10.1093/emboj/cdf301 · DOI
- Briegel, 1993, Genes Dev., 7, 1097, 10.1101/gad.7.6.1097 · DOI
- Perry, 2002, Eur. J. Biochem., 269, 3607, 10.1046/j.1432-1033.2002.02999.x · DOI
- Ferreira, 2005, Mol. Cell. Biol., 25, 1215, 10.1128/MCB.25.4.1215-1227.2005 · DOI
- Fan, 2002, J. Immunol., 168, 755, 10.4049/jimmunol.168.2.755 · DOI
- Dickson, 1995, Development, 121, 1845, 10.1242/dev.121.6.1845 · DOI · Paper page
- Zermati, 2000, Exp. Hematol., 28, 256, 10.1016/S0301-472X(99)00155-1 · DOI
- Zermati, 2000, Exp. Hematol., 28, 885, 10.1016/S0301-472X(00)00488-4 · DOI
- Bai, 2010, Cell, 142, 133, 10.1016/j.cell.2010.05.028 · DOI
- Sato, 2008, Cancer Sci., 99, 1407, 10.1111/j.1349-7006.2008.00842.x · DOI
- Wang, 2011, Mol. Syst. Biol., 7, 536, 10.1038/msb.2011.67 · DOI
- Itoh, 2000, Eur. J. Biochem., 267, 6954, 10.1046/j.1432-1327.2000.01828.x · DOI
- Ozawa, 2001, Blood, 98, 2116, 10.1182/blood.V98.7.2116 · DOI
- Fukuchi, 2001, Oncogene, 20, 704, 10.1038/sj.onc.1204142 · DOI
- Massague, 2000, Genes Dev., 14, 627, 10.1101/gad.14.6.627 · DOI
- Akiyoshi, 1999, J. Biol. Chem., 274, 35269, 10.1074/jbc.274.49.35269 · DOI
- Erickson, 2009, Mol. Biol. Cell, 20, 1509, 10.1091/mbc.E08-08-0836 · DOI
- Choi, 2005, Mol. Cell. Biochem., 271, 23, 10.1007/s11010-005-3456-7 · DOI · Paper page
- Chiba, 2003, Proc. Natl. Acad. Sci. U. S. A., 100, 15577, 10.1073/pnas.2536757100 · DOI
- Moustakas, 2001, J. Cell Sci., 114, 4359, 10.1242/jcs.114.24.4359 · DOI
- Fortunel, 2000, Blood, 96, 2022, 10.1182/blood.V96.6.2022 · DOI
- Kamesaki, 1996, Blood, 87, 999, 10.1182/blood.V87.3.999.bloodjournal873999 · DOI
- Attisano, 2002, Science, 296, 1646, 10.1126/science.1071809 · DOI
- Wakefield, 2002, Curr. Opin. Genet. Dev., 12, 22, 10.1016/S0959-437X(01)00259-3 · DOI
- Massague, 2000, Nat. Rev. Mol. Cell Biol., 1, 169, 10.1038/35043051 · DOI
- Kumar, 2012, Cell, 149, 642, 10.1016/j.cell.2012.02.059 · DOI
Cited by
Sorted by citations
Frye, M., Taddei, A., Dierkes, C., Martinez-Corral, I., Fielden, M., Ortsäter, H., Kazenwadel, J., Calado, D. P., Ostergaard, P., Salminen, M., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-03959-6 · Cited by 169
Red Blood Cells as Potential Repositories of MicroRNAs in the Circulatory System
Sun, L., Yu, Y., Niu, B., & Wang, D. (2020) · Frontiers in Genetics · doi:10.3389/fgene.2020.00442 · Cited by 83
Metadata
- Authors
- Dong, X.-M., Yin, R.-H., Yang, Y., Feng, Z.-W., Ning, H.-M., Dong, L., Zheng, W.-W., Tang, L.-J., Wang, J., Jia, Y.-X., Jiang, Y.-N., Liu, E.-D., Chen, H., Zhan, Y.-Q., Yu, M., Ge, C.-H., Li, C.-Y., & Yang, X.-M.
- Venue
- Cellular Signalling
- Publisher
- Elsevier BV
- Published
- 2014-05
- Volume
- 26
- Issue
- 5
- Pages
- 1089-1097
- ISSN
- 0898-6568
- Cited by
- 19
- References
- 1
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: GATA-2 inhibits transforming growth factor-β signaling pathway through interaction with Smad4. https://app.cochat.ai/papers/10.1016/j.cellsig.2014.01.028
- The paper
- Dong, X.-M., Yin, R.-H., Yang, Y., Feng, Z.-W., Ning, H.-M., Dong, L., Zheng, W.-W., Tang, L.-J., Wang, J., Jia, Y.-X., Jiang, Y.-N., Liu, E.-D., Chen, H., Zhan, Y.-Q., Yu, M., Ge, C.-H., Li, C.-Y., & Yang, X.-M. (2014). GATA-2 inhibits transforming growth factor-β signaling pathway through interaction with Smad4. Cellular Signalling. https://doi.org/10.1016/j.cellsig.2014.01.028