Investigating the Role of mSlap2 in Gfi1-mediated Inhibition of Erk1/2

Gfi1 is known as a nuclear transcriptional repressor that positively regulates B and T cell development and is required for the development of granulocytes. Gfi1 supports granulocyte differentiation at the expense of monocyte differentiation by repressing genes encoding Monocyte-Colony Stimulating Factor (M-CSF) and PU.1, which favor monocyte differentiation. However, the molecular mechanisms by which Gfi1 acts in myeloid development remain incompletely understood. For instance, in contrast to a previous publication reporting that Gfi1 increased the activation of Erk1/2, Dr. Dong’s lab has recently found that Gfi1 inhibits Erk1/2 phosphorylation/activation. The exact pathway leading to Gfi1-mediated inhibition of Erk1/2 activation is yet to be elucidated. Since Gfi1 is a nuclear transcription factor, it is possible that Gfi1 may inhibit Erk1/2 activation by regulating the expression of a cytoplasmic regulator of Erk1/2 activation. In preliminary data obtained from Dr. Dong’s lab, Gfi1 was shown to upregulate the expression of mSlap2. Interestingly, mSlap2 is a cytoplasmic protein that has been shown to inhibit the activation of Erk1/2. We hypothesize that mSlap2 may play a key role in Gfi1-mediated inhibition of Erk1/2 activation in response to Granulocyte-Colony Stimulating Factor (G-CSF).
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Abstract/Description: Gfi1 is known as a nuclear transcriptional repressor that positively regulates B and T cell development and is required for the development of granulocytes. Gfi1 supports granulocyte differentiation at the expense of monocyte differentiation by repressing genes encoding Monocyte-Colony Stimulating Factor (M-CSF) and PU.1, which favor monocyte differentiation. However, the molecular mechanisms by which Gfi1 acts in myeloid development remain incompletely understood. For instance, in contrast to a previous publication reporting that Gfi1 increased the activation of Erk1/2, Dr. Dong’s lab has recently found that Gfi1 inhibits Erk1/2 phosphorylation/activation. The exact pathway leading to Gfi1-mediated inhibition of Erk1/2 activation is yet to be elucidated. Since Gfi1 is a nuclear transcription factor, it is possible that Gfi1 may inhibit Erk1/2 activation by regulating the expression of a cytoplasmic regulator of Erk1/2 activation. In preliminary data obtained from Dr. Dong’s lab, Gfi1 was shown to upregulate the expression of mSlap2. Interestingly, mSlap2 is a cytoplasmic protein that has been shown to inhibit the activation of Erk1/2. We hypothesize that mSlap2 may play a key role in Gfi1-mediated inhibition of Erk1/2 activation in response to Granulocyte-Colony Stimulating Factor (G-CSF).
Subject(s): hematology; Gfi1; M-CSF; G-CSF; B cells; T cells; monocytes; granulocytes; Erk1/2; mSlap2
Title: Investigating the Role of mSlap2 in Gfi1-mediated Inhibition of Erk1/2.
Name(s): Grim, Allison, author
Dong, Fan, author
Dr. Fan Dong, advisor
Type of Resource: text
Genre: poster
Other Date: 2018-03-23
Physical Form: application/pdf
Extent: 1 p.
Abstract/Description: Gfi1 is known as a nuclear transcriptional repressor that positively regulates B and T cell development and is required for the development of granulocytes. Gfi1 supports granulocyte differentiation at the expense of monocyte differentiation by repressing genes encoding Monocyte-Colony Stimulating Factor (M-CSF) and PU.1, which favor monocyte differentiation. However, the molecular mechanisms by which Gfi1 acts in myeloid development remain incompletely understood. For instance, in contrast to a previous publication reporting that Gfi1 increased the activation of Erk1/2, Dr. Dong’s lab has recently found that Gfi1 inhibits Erk1/2 phosphorylation/activation. The exact pathway leading to Gfi1-mediated inhibition of Erk1/2 activation is yet to be elucidated. Since Gfi1 is a nuclear transcription factor, it is possible that Gfi1 may inhibit Erk1/2 activation by regulating the expression of a cytoplasmic regulator of Erk1/2 activation. In preliminary data obtained from Dr. Dong’s lab, Gfi1 was shown to upregulate the expression of mSlap2. Interestingly, mSlap2 is a cytoplasmic protein that has been shown to inhibit the activation of Erk1/2. We hypothesize that mSlap2 may play a key role in Gfi1-mediated inhibition of Erk1/2 activation in response to Granulocyte-Colony Stimulating Factor (G-CSF).
Identifier(s): 2017_scholcel_allisongrim_mSlap2 (IID)
Subject(s): hematology; Gfi1; M-CSF; G-CSF; B cells; T cells; monocytes; granulocytes; Erk1/2; mSlap2
Held by: University of Toledo Digital Repository
Location: University of Toledo Digital Repository
Rights Statement: http://rightsstatements.org/vocab/InC/1.0/ -- In Copyright
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