FIGURE

Fig. 6

ID

ZDB-FIG-140710-48

Publication

Bu et al., 2014 - Protein tyrosine phosphatase PTPN9 regulates erythroid cell development through STAT3 dephosphorylation in zebrafish

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Fig. 6

Overexpressing gata1, zbp-89 or dominant-negative STAT3 rescues erythroid development in ptpn9a-morphant embryos and PTPN9-knockdown K562 cells. (A-C,G-L) βe1-globin was partially rescued in ptpn9a morphants (MO) that had been co-injected with gata1 mRNA (C), zbp-89 mRNA (I) or dominant-negative STAT3 (STAT3DN) mRNA (L), compared with wild-type (WT) controls (A,G,J) at 48 hpf. In addition, overexpression of gata1 mRNA rescued primitive erythrocytes in ptpn9a morphants (F), compared with wild-type controls (D), as revealed by o-Dianisidine staining. The numbers in the bottom left corner represent phenotypic embryos/total embryos. (M-P) Overexpression of STAT3DN rescued benzidine-positive erythroids (M) and γ-globin (N), CD235a (O) and CD71 (P) expression in K562 cells that had been infected with either mutant PTPN9 (N9CS) or transfected with PTPN9 shRNA (shN9) after induction with hemin for 48h, compared with vector (Vec) or scrambled (Scr) controls. The data represent the means of three independent experiments±s.d., *P<0.05.

Expression Data

Gene:	hbbe1.1
Fish:	WT WT + MO1-ptpn9a
Knockdown Reagent:	MO1-ptpn9a
Anatomical Term:	erythroid lineage cell
Stage:	Long-pec

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	WT + MO1-ptpn9a
Knockdown Reagent:	MO1-ptpn9a
Observed In:	blood cell
Stage:	Long-pec

Phenotype Detail

Acknowledgments

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