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PMID |
Sentence |
1 |
7568026
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Both Stat5a and Stat5b recognized the GAS site (gamma-interferon-activating sequence; TTCNNNGAA) in vitro and mediated PRL-induced transcription in COS cells transfected with a PRL receptor.
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2 |
7568026
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Stat5b also induced basal transcription in the absence of PRL.
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3 |
15749807
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In the present work, total STAT5B and STAT1 protein levels were not altered by prolonged insulin treatment.
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4 |
16306356
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Leptin stimulation led to janus kinase (JAK)2-dependent phosphorylation and nuclear translocation of the transcription factors signal transducer and activator of transcription (STAT)3 and STAT5b in INS-1 beta-cells.
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5 |
16306356
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Transcriptional activation of the rat SOCS3 promoter by leptin was observed with concomitant leptin-induced STAT3 and STAT5b DNA binding to specific promoter regions.
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6 |
16505237
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To our surprise, the binding ability of Stat5b is inconsistent with the presence or absence of the Stat5b mutation in these congenic mice but is correlated with the expression levels of the Crkl protein, which was coprecipitated by an anti-Stat5b antibody.
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7 |
16505237
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Both the expression of Crkl and the Stat5b binding ability are the highest in B6.NOD-c11 and the lowest in NOD while intermediate in B6 and NOD.Lc11 mice.
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8 |
16505237
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We demonstrated that the adapter molecule Crkl can bind Stat5b and that the Crkl protein is a Stat5b binding cofactor.
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9 |
16505237
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More importantly, profection of Crkl recombinant protein significantly increased Stat5b binding ability and rescued the binding defect of the NOD mutant Stat5b, suggesting that Crkl is a key regulatory molecule for Stat5b binding.
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10 |
16505237
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Therefore, the defective Crkl expression may contribute to the development of diabetes in the NOD mice by exacerbating the defective Stat5b binding ability.
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11 |
21166888
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Human recombinant GH stimulated JAK2 and STAT5b tyrosine phosphorylation and IGF-I production in a concentration-dependent manner.
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12 |
21592969
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It has been shown that the transcription factor Stat5b mediates the GH promoting effect on IGF-1 expression and on chondrogenesis, yet it is not known whether other signaling molecules are activated by GH in growth plate chondrocytes.
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13 |
21592969
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Lastly, the inhibition of Stat5b expression in chondrocytes prevented the GH promoting effects on NF-?B-DNA binding, whereas the inhibition of NF-?B p65 expression or activity prevented the GH-dependent activation of IGF-1 and bone morphogenetic protein-2 expression.
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