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AKT phosphorylates GATA1. 18 / 18
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"Furthermore, Akt directly phosphorylated and activated the transcription factor GATA-1 (Globin transcription factor-1), a key regulator of erythroid differentiation [121–123] ."

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"In the context of EPO signaling it has been shown that Akt phosphorylates both GATA-1 and Foxo3a, transcription factors of crucial importance in erythropoiesis ( Bouscary et al., 2003; Kadri et al., 2[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"During EPO stimulation of erythroid progenitor cells, AKT activation is required for erythroid differentiation and increases phosphorylation of GATA-1 and enhances GATA-1 activity to upregulate red blood cell gene expression including EPOR (Chin et al., 1995, Zhao et al., 2006)."

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"Protein Kinase B (AKT) can phosphorylate FOXO1 and GATA1 and regulate their transcriptional activity to MMP9 and TIMP-1 (Figure 4)."

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"In the context of EPO signaling it has been shown that Akt phosphorylates both GATA-1 and Foxo3a, transcription factors of crucial importance in erythropoiesis ( Bouscary et al., 2003; Kadri et al., 2[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Protein Kinase B (AKT) can phosphorylate FOXO1 and GATA1 and regulate their transcriptional activity to MMP9 and TIMP-1 ( xref )."

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"Of these, JAK2-STAT5 activates Bcl-xL to prevent apoptosis of erythroid progenitors, whereas Akt promotes differentiation by phosphorylating the essential erythroid transcription factor GATA1 and activating metabolic pathways via phosphorylation of the mTORC1 complex."

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"Among its pleiotropic effects on erythroid cells, EPO induced Akt activation promotes differentiation because Akt phosphorylates and activates GATA1, providing a possible explanation for our observation that inhibition of Akt activity is associated with truncated differentiation."

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"Therefore, these results suggest that gastrodin stimulates the PI3K/AKT pathway and that activation of the PI3K/AKT pathway promotes USP4 expression by enhancing the phosphorylation of GATA1 in HepG2 cells."

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"Coincidentally, and in support of our findings, AKT was found to synchronize cell proliferation and differentiation during erythropoiesis by phosphorylating GATA1, thereby increasing its affinity for FOG1 (Kadri et al., 2015)."

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"AKT has previously been shown to induce TIMP-1 expression by directly phosphorylating and activating GATA1."

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"However, following a mutation in GATA-1 (such as V205M), the amino acid is not phosphorylated by AKT, resulting in disrupted formation of GATA-1: FOG-1 complex (Table 1 )."

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"PI3K and AKT stimulates the phosphorylation and activation of GATA1 [XREF_BIBR], and activated GATA-1 upregulates its own gene expression through positive feedback regulation [XREF_BIBR]."

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"It has been reported that the activation of the PI3K/AKT pathway induces the phosphorylation of GATA-1 (Zhao et al., 2006)."

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"Among its pleiotropic effects on erythroid cells, EPO-induced Akt activation promotes differentiation because Akt phosphorylates and activates GATA1 ( xref ), providing a possible explanation for our observation that inhibition of Akt activity is associated with truncated differentiation."

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"Akt phosphorylates the transcription factor GATA binding protein-1 (GATA-1), which is an important transcription factor for the anti-apoptotic Bcl-X expression and erythroid-specific genes."

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"AKT phosphorylates GATA-1 in erythroid cells XREF_BIBR and K562 cells XREF_BIBR resulting in an increase in its DNA binding affinity and enhanced transcriptional activity."

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"AKT phosphorylates GATA-1 in erythroid cells xref and K562 cells xref resulting in an increase in its DNA-binding affinity and enhanced transcriptional activity."