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MRNA expression of CD163 (left panal) and M1 polarization was evaluated by HLA-DRA mRNA expression (right panal). b Explant mammary gland sections were subjected to immunohistochemical analysis, stained for CD163 (left panel) or HLA-DRA (right panel) and images were captured at 100X. Representative pictures are displayed for tissues from each treatment group which was performed in triplicate sampl
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MRNA expression of CD163 (left panal) and M1 polarization was evaluated by HLA-DRA mRNA expression (right panal). b Explant mammary gland sections were subjected to immunohistochemical analysis, stained for CD163 (left panel) or HLA-DRA (right panel) and images were captured at 100X. Representative pictures are displayed for tissues from each treatment group which was performed in triplicate sampl
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MRNA expression of CD163 (left panal) and M1 polarization was evaluated by HLA-DRA mRNA expression (right panal). b Explant mammary gland sections were subjected to immunohistochemical analysis, stained for CD163 (left panel) or HLA-DRA (right panel) and images were captured at 100X. Representative pictures are displayed for tissues from each treatment group which was performed in triplicate sampl
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MRNA expression of CD163 (left panal) and M1 polarization was evaluated by HLA-DRA mRNA expression (right panal). b Explant mammary gland sections were subjected to immunohistochemical analysis, stained for CD163 (left panel) or HLA-DRA (right panel) and images were captured at 100X. Representative pictures are displayed for tissues from each treatment group which was performed in triplicate sampl
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He National Institutes of Health. The protocol was approved by the Baystate Medical Center Institutional Animal Care and Use Committee (Permit Number: 132-681).8. 9.10.11.12. 13.14.15.16.17.Publisher's NoteSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Author details 1 Pioneer Valley Life Sciences Institute, Baystate Medical C
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Imulates and TGFBR inhibition represses EGR2 mRNA expression in both HMECs as well as MMECs (Additional file 2: Figure S2, Fig. 2). We have also observed that tumors derived from Sfrp1-/- mice express significantly higher levels of both Tgfb1 and Egr2 mRNA (data not shown). Dillon et al. revealed that Egr2 expression is upregulated in Erbb2 driven mammary tumors [25]. However, these researchers di
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Imulates and TGFBR inhibition represses EGR2 mRNA expression in both HMECs as well as MMECs (Additional file 2: Figure S2, Fig. 2). We have also observed that tumors derived from Sfrp1-/- mice express significantly higher levels of both Tgfb1 and Egr2 mRNA (data not shown). Dillon et al. revealed that Egr2 expression is upregulated in Erbb2 driven mammary tumors [25]. However, these researchers di
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Line resulted in decreased EGR2 expression (26). Chandra et al. demonstrate that the MAPK/ERK pathway is a major downstream signaling pathway mediating the stimulatory effects of EGF on EGR2 expression and osteoprogenitor survival [28]. Finally, To et al. report that the same MEK inhibitor utilized in our experiments, U0126, was the elicited the most potent inhibition of EGR2 transcription in brea
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Imulates and TGFBR inhibition represses EGR2 mRNA expression in both HMECs as well as MMECs (Additional file 2: Figure S2, Fig. 2). We have also observed that tumors derived from Sfrp1-/- mice express significantly higher levels of both Tgfb1 and Egr2 mRNA (data not shown). Dillon et al. revealed that Egr2 expression is upregulated in Erbb2 driven mammary tumors [25]. However, these researchers di
1
Line resulted in decreased EGR2 expression (26). Chandra et al. demonstrate that the MAPK/ERK pathway is a major downstream signaling pathway mediating the stimulatory effects of EGF on EGR2 expression and osteoprogenitor survival [28]. Finally, To et al. report that the same MEK inhibitor utilized in our experiments, U0126, was the elicited the most potent inhibition of EGR2 transcription in brea