PMID 12783775, 12754525 are not in MGI as of now. Do you mean you think these papers may be used to add "regulation of gluconeogenesis" (GO:0006111) annotations to mouse gene Foxo1?
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From these statements in the abstracts, I'd say yes:
PMID 12783775: "a Foxo1 mutant (Foxo1-Delta256), devoid of its carboxyl domain, has been shown to interfere with Foxo1 function and inhibit gluconeogenic gene expression in cultured cells."
PMID 12754525: "FOXO1 function is required for the robust activation of gluconeogenic gene expression in hepatic cells and in mouse liver by PGC-1alpha."
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I would say yes...from the first paper: "We showed that hepatic production of Foxo1-{Delta}256 inhibited both PEPCK and G-6-Pase, but not GAPDH, expression in H4IIE cells."
PEPCK and G-6-Pase are both constituent functions in gluconeogenesis, and FoxO1 is regulating their presence, therefore it is a 'positive regulation of gluconeogenesis'.
Do you agree? I might use this one for the regulation discussion at the annotation camp next week.
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PMID:12783775 PMID: 11696581 PMID: 12754525
There are many papers indexed to Foxo1 in MGI, however, we didn’t get a chance to annotate them yet, and MGI references happen to be not including these three. I just made a internal request to add them into our system.
By reading the first paper, I think we can annotate Foxo1 to "positive regulation of gluconeogenesis" base on the two-piece of information from the paper:
1. hepatic production of Foxo1- 256 significantly reduced the degree of hyperglycemia (from >500 mg/dl to 283 ± 40 mg/dl) 3 days after vector administration.
2. the expression levels of PEPCK and G-6-Pase mRNAs relative to that of -actin mRNA were significantly decreased in response to hepatic Foxo1- 256 expression in the mouse liver tissue…
The sentence Jean used from the abstract is actually talking about over-expression of a mutant mouse protein: a dominant-negative FOXO1 (1–256) at a RAT cell line (H4IIE) system, I already respond to her separately.
As I talked with David this morning, at MGI, we usually don’t use expression change only data to do GO annotation. For example, if a mutation of a transcriptional factor cause 20 genes’ expression change, we do not come in categorize the 20 targets and annotate the TF to the processes that these targets might involve in. Since in this paper there is also evidence of hyperglycemia, I think we can annotate Foxo1 to "positive regulation of gluconeogenesis". I will add the annotation to MGI as soon as the paper being added to our system, it will probably be sometime next week.
Thanks,
Li
If you would like to refer to this comment somewhere else in this project, copy and paste the following link:
PMID 12783775, 12754525 are not in MGI as of now. Do you mean you think these papers may be used to add "regulation of gluconeogenesis" (GO:0006111) annotations to mouse gene Foxo1?
From these statements in the abstracts, I'd say yes:
PMID 12783775: "a Foxo1 mutant (Foxo1-Delta256), devoid of its carboxyl domain, has been shown to interfere with Foxo1 function and inhibit gluconeogenic gene expression in cultured cells."
PMID 12754525: "FOXO1 function is required for the robust activation of gluconeogenic gene expression in hepatic cells and in mouse liver by PGC-1alpha."
I would say yes...from the first paper: "We showed that hepatic production of Foxo1-{Delta}256 inhibited both PEPCK and G-6-Pase, but not GAPDH, expression in H4IIE cells."
PEPCK and G-6-Pase are both constituent functions in gluconeogenesis, and FoxO1 is regulating their presence, therefore it is a 'positive regulation of gluconeogenesis'.
Do you agree? I might use this one for the regulation discussion at the annotation camp next week.
PMID:12783775 PMID: 11696581 PMID: 12754525
There are many papers indexed to Foxo1 in MGI, however, we didn’t get a chance to annotate them yet, and MGI references happen to be not including these three. I just made a internal request to add them into our system.
By reading the first paper, I think we can annotate Foxo1 to "positive regulation of gluconeogenesis" base on the two-piece of information from the paper:
1. hepatic production of Foxo1- 256 significantly reduced the degree of hyperglycemia (from >500 mg/dl to 283 ± 40 mg/dl) 3 days after vector administration.
2. the expression levels of PEPCK and G-6-Pase mRNAs relative to that of -actin mRNA were significantly decreased in response to hepatic Foxo1- 256 expression in the mouse liver tissue…
The sentence Jean used from the abstract is actually talking about over-expression of a mutant mouse protein: a dominant-negative FOXO1 (1–256) at a RAT cell line (H4IIE) system, I already respond to her separately.
As I talked with David this morning, at MGI, we usually don’t use expression change only data to do GO annotation. For example, if a mutation of a transcriptional factor cause 20 genes’ expression change, we do not come in categorize the 20 targets and annotate the TF to the processes that these targets might involve in. Since in this paper there is also evidence of hyperglycemia, I think we can annotate Foxo1 to "positive regulation of gluconeogenesis". I will add the annotation to MGI as soon as the paper being added to our system, it will probably be sometime next week.
Thanks,
Li
Pos. reg. noted in MGI. Thanks!