Effect of SOCS2 R96C mutation on mouse mammary gland development and function
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ABSTRACT:
PROVIDER: PRJNA935704 | ENA |
REPOSITORIES: ENA
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Project description:The R96C mutation in SOCS2 (suppressor of cytokine signaling 2) that leads to greater milk production but also a greater sensitivity to mastitis was identified in Lacaune sheep by Rupp et al, 2015. This mutation leads to a loss of ligand recognition for SOCS2 and thus interferes with JAK/STAT signaling pathway regulation. A mouse model carrying this mutation (SOCS2 R96C KI) was developed to study its effects on mammary gland development and lactation.
2024-02-26 | GSE225441 | GEO
Project description:The goal of this study is to improve the quality, efficiency, and sustainability of milk production by improving the understanding of the function of cis-regulatory elements in regulating the bovine mammary gland. To this end, we have characterized the non-lactating and lactating mammary gland transcriptomes by whole transcriptome shotgun sequencing (RNA-seq). We will identify cis-regulatory elements in the non-lactating and lactating bovine mammary gland genome-wide. Finally, we will annotate and characterize mammary gland cis-regulatory elements by computational analysis and identify high-resolution genome-wide in vivo footprints of diverse trans-acting-factors (TF), over-represented TF bindings sites and overlapping SNPs.
2021-04-06 | GSE116079 | GEO
Project description:Characterizing cis-regulatory elements associated with mammary gland function
| PRJNA476965 | ENA
Project description:SOCS2 Ensures Metabolic Function and Mass Restoration During Liver Regeneration - SOCS2 plays distinct and contrasting roles during liver regeneration. Early after injury, SOCS2 expression increases and limits the rate of regeneration, preserving metabolic activity. Surprisingly, at later times, the role of SOCS2 reverses to promote liver regeneration by stimulating GH release from the pituitary via effects on serum levels of insulin-like growth factor 1. Loss of SOCS2 promotes GH signaling by increasing growth hormone receptor levels and driving phosphorylation of proteins in the GH pathway, establishing a state of hyper-responsiveness to GH. These findings suggest a single protein can play contrasting roles at different times after liver injury and modulation of GH signaling achieves an optimal rate of liver regeneration to balance metabolic and restorative needs. To further understand the mechanism by which SOCS2 increases early liver regeneration, we performed microarray analysis of Socs2-null mice wildtype mice at 24 and 36 hours after hepatectomy. C57BL/6 mice where used as wildtype controls. Socs2-null animals were maintained on a C57BL/6 background. Both wildtype and Socs2-null adult mice were subjected to 2/3 hepatectomy and liver tissue isolated at 24 hours and 36 hours post hepatectomy. Time zero was without hepatectomy in age-matched mice for each genotype. Total RNA isolated from collected liver tissues was pooled for three animals at each time point and two biological replicates (3 pooled liver RNAs each) were labeled for array analysis. This results in a total of 12 microarrays.
2014-02-01 | E-GEOD-51801 | biostudies-arrayexpress
Project description:SOCS2 Ensures Metabolic Function and Mass Restoration During Liver Regeneration - SOCS2 plays distinct and contrasting roles during liver regeneration. Early after injury, SOCS2 expression increases and limits the rate of regeneration, preserving metabolic activity. Surprisingly, at later times, the role of SOCS2 reverses to promote liver regeneration by stimulating GH release from the pituitary via effects on serum levels of insulin-like growth factor 1. Loss of SOCS2 promotes GH signaling by increasing growth hormone receptor levels and driving phosphorylation of proteins in the GH pathway, establishing a state of hyper-responsiveness to GH. These findings suggest a single protein can play contrasting roles at different times after liver injury and modulation of GH signaling achieves an optimal rate of liver regeneration to balance metabolic and restorative needs. To further understand the mechanism by which SOCS2 increases early liver regeneration, we performed microarray analysis of Socs2-null mice wildtype mice at 24 and 36 hours after hepatectomy.
2014-02-01 | GSE51801 | GEO
Project description:miRNAs are not well known their expression and function in mammary gland development. To identify the miRNAs expression during mammary gland development, mammary bud were dissected at E13.5
2015-03-06 | GSE66546 | GEO
Project description:Identify gene expression changes in the absence of Plk2 Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis. Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis.
2014-05-20 | GSE50003 | GEO
Project description:Identify gene expression changes in the absence of Plk2 Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis. Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis. Comparison between Plk2 +/+ (n=3) and Plk2 -/- (n=3) mouse mammary epithelial cells
2014-05-20 | E-GEOD-50003 | biostudies-arrayexpress
Project description:To study the effects of Rac1 gene deletion on development and function of the mammary gland.
2016-11-01 | GSE85188 | GEO