Human Mammary Cell Resource.

1997 ◽  
Author(s):  
Martha R. Stampfer
Keyword(s):  
Mammary Cell

GENE ACTIVATION IN MAMMARY CELLS

1972 ◽  
Vol 71 (2_Suppla) ◽  
pp. S346-S368 ◽  
Author(s):  
Roger W. Turkington ◽  
Nobuyuki Kadohama
Keyword(s):  
Cell Differentiation ◽  
Gene Transcription ◽  
Hormonal Regulation ◽  
Gene Activation ◽  
Milk Proteins ◽  
Mouse Mammary Gland ◽  
Nuclear Proteins ◽  
Mammary Cells ◽  
Alveolar Cells ◽  
Mammary Cell

ABSTRACT Hormonal activation of gene transcription has been studied in a model system, the mouse mammary gland in organ culture. Transcriptive activity is stimulated in mammary stem cells by insulin, and in mammary alveolar cells by prolactin and insulin. Studies on the template requirement for expression of the genes for milk proteins demonstrate that DNA methylation has an obligatory dependence upon DNA synthesis, but is otherwise independent from hormonal regulation of mammary cell differentiation. Incorporation of 5-bromo-2′deoxyuridine into DNA selectively inhibits expression of the genes for specific milk proteins. Undifferentiated mammary cells activate the synthesis of specific acidic nuclear proteins when stimulated by insulin. Several of these induced acidic nuclear proteins are undetectable in unstimulated undifferentiated cells, but appear to be characteristic components of the nuclei of differentiated cells. These results indicate that mammary cell differentiation is associated with a change in acidic nuclear proteins, and they provide evidence to support the concept that acidic nuclear proteins may be involved in the regulation of gene transcription and of mammary cell differentiation.

scholarly journals Mammary Cell Number, Proliferation, and Apoptosis During a Bovine Lactation: Relation to Milk Production and Effect of bST

2001 ◽  
Vol 84 (10) ◽  
pp. 2177-2187 ◽  
Author(s):  
A.V. Capuco ◽  
D.L. Wood ◽  
R. Baldwin ◽  
K. Mcleod ◽  
M.J. Paape
Keyword(s):  
Milk Production ◽  
Cell Number ◽  
Mammary Cell ◽  
Proliferation And Apoptosis

scholarly journals Laminin 332 expression in mammary cell lines

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Philip M Carpenter ◽  
Gary K Ohanian ◽  
Zesong Zhang ◽  
Meghedy Shanazarian ◽  
Harut Madatovian
Keyword(s):  
Cell Lines ◽  
Mammary Cell ◽  
Laminin 332

scholarly journals Glucocorticolds and mammary gland development : mammary cell multiplication and hypertrophy in rabbit

1978 ◽  
Vol 18 (6) ◽  
pp. 1325-1331 ◽  
Author(s):  
J. FÈVRE ◽  
L.-M. HOUDEBINE ◽  
Nicole VERMEIRE ◽  
B. MORET ◽  
Claudine PUISSANT
Keyword(s):  
Mammary Gland ◽  
Mammary Gland Development ◽  
Cell Multiplication ◽  
Mammary Cell ◽  
Gland Development

scholarly journals MYC regulates a pan-cancer network of co-expressed oncogenic splicing factors

2021 ◽  
Author(s):  
Laura Urbanski ◽  
Mattia Brugiolo ◽  
SungHee Park ◽  
Brittany L Angarola ◽  
Nathan K Leclair ◽  
...  
Keyword(s):  
Attractive Alternative ◽  
Splicing Factors ◽  
Multiple Tumor ◽  
Alternative Mrna Splicing ◽  
Mammary Cell ◽  
Effector Pathways ◽  
And Function ◽  
Tumor Types ◽  
Cancer Network ◽  
Pan Cancer

MYC is dysregulated in >50% of cancers, but direct targeting of MYC has been clinically unsuccessful. Targeting downstream MYC effector pathways represents an attractive alternative. MYC regulates alternative mRNA splicing, a hallmark of cancer, but the mechanistic links between MYC and the splicing machinery remain underexplored. Here, we identify a network of splicing factors (SFs) co-expressed as SF-modules in MYC-active breast tumors. Of these, one is a pan-cancer SF-module, correlating with MYC-activity across 33 tumor types. In mammary cell models, MYC activation leads to co-upregulation of pan-cancer module SFs and to changes in >4,000 splicing events. In breast cancer organoids, co-overexpression of the pan-cancer SF-module is sufficient to induce splicing events that are also MYC-regulated in patient tumors and to increase organoid size and invasiveness, while its knockdown decreases organoid size. Finally, we uncover a pan-cancer splicing signature of MYC activity which correlates with survival in multiple tumor types. Our findings provide insight into the mechanisms and function of MYC-regulated splicing and for the development of therapeutics for MYC-driven tumors.

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