Null mutation of the prolactin receptor gene produces multiple reproductive defects in the mouse.

Ormandy, Christopher J.; Camus, Anne; Barra, Jacqueline; Damotte, Diane; Lucas, Brian K.; Buteau, Hélène; Edery, Marc; Brousse, Nicole; Babinet, Charles; Binart, Nadine; Kelly, Paul A.

doi:10.1101/gad.11.2.167

Cited by 711 publications

(465 citation statements)

References 79 publications

(54 reference statements)

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“…Presumably, the reduced levels of Stat5b were capable of sustaining expression of other milk protein genes, providing evidence for discrete functions for these highly related transcription factors. Overall, the mammary develop phenotype of Stat5a-de®cient mice resembled that of prolactin receptor de®cient mice (Ormandy et al, 1997), suggesting that Stat5a is indispensable for this aspect of prolactin function.…”

Section: Stat5mentioning

confidence: 91%

Divergent roles of STAT1 and STAT5 in malignancy as revealed by gene disruptions in mice

Levy

Gilliland

2000

Oncogene

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Section: Stat5mentioning

confidence: 91%

Divergent roles of STAT1 and STAT5 in malignancy as revealed by gene disruptions in mice

Levy

Gilliland

2000

Oncogene

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“…Prlr 2/2 mice were backcrossed for .12 generations into 129P2/Ola background (24). Prl 2/2 B6.129S2(Cg)-Prl tm1Hmn /J mice backcrossed for 10 generation into C57BL/6 background were purchased from Jackson Laboratories (25).…”

Section: Micementioning

confidence: 99%

“…Heterozygous pairs of each strain were bred to obtain Prlr 2/2 and Prlr +/+ or Prl 2/2 and Prl +/+ mice. Genotyping was performed by PCR in Prlr 2/2 and Prlr +/+ as previously described (24) and in Prl 2/2 and Prl +/+ as recommended by the vendor. C57BL/6 mice were from Charles River.…”

Section: Micementioning

confidence: 99%

Prolactin Is Not Required for the Development of Severe Chronic Experimental Autoimmune Encephalomyelitis

Costanza

Musio

Abou-Hamdan

et al. 2013

The Journal of Immunology

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Predominance of multiple sclerosis (MS) in women, reductions of disease flares during pregnancy, and their increase in the postpartum period have suggested a hormonal influence on MS activity. The hormone prolactin (PRL) has long been debated as a potential immune-stimulating factor in several autoimmune disorders, including MS and its animal model experimental autoimmune encephalomyelitis (EAE). However, to date, no data clearly ascribe a pathogenic role to PRL in these diseases. Using PRL receptor–deficient (Prlr−/−) and PRL-deficient (Prl−/−) mice, we show that PRL plays a redundant role in the development of chronic EAE. In Prlr−/− and Prl−/− mice, EAE developed with a delayed onset compared with littermate control mice, but with full clinical severity. In line with the clinical outcome, T cell proliferation and production of IFN-γ, IL-17A, and IL-6 induced by myelin Ag were delayed in Prlr−/− and Prl−/− mice. Ag-specific IgG Ab responses were not affected by PRLR or PRL deficiency. We also show that mouse lymph node cells and purified CD4+ T cells express transcript for Prlr, but not for Prl. These results reveal that PRL does not play a central role in the development of chronic EAE and optimal Th1 and Th17 responses against myelin. Moreover, they also rule out a possible contribution of PRL secreted by immune cells to the modulation of autoreactive T cell response in this model.

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“…In the case of the prolactin receptor, heterozygous mice displayed severely impaired lobuloalveolar development resulting in a failure to lactate after the first pregnancy, indicating a threshold level of prolactin receptor is necessary for proper development (Ormandy et al 1997). The ability of the females to successfully nurse after successive pregnancies was directly related to the degree of lobuloalveolar development observed, presumably because of varying expression levels of the prolactin receptor.…”

Section: Potential C/ebp␤ Target Genes In the Mammary Glandmentioning

confidence: 99%

C/EBPβ, but not C/EBPα, is essential for ductal morphogenesis, lobuloalveolar proliferation, and functional differentiation in the mouse mammary gland

Seagroves¹,

Krnacik²,

Raught³

et al. 1998

Genes Dev.

234

207

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The CCAAT/enhancer binding proteins (C/EBPs) are differentially expressed throughout mammary gland development and interact with binding sites within the promoter of a milk protein gene, ␤-casein. The specific roles of C/EBP␤ and C/EBP␣ in mouse mammary gland development and differentiation have been investigated in mice that carry targeted deletions of these genes. C/EBP␤ −/− virgin mice exhibited cystic, enlarged mammary ducts with decreased secondary branching. Transplantation of C/EBP␤ −/− mammary epithelium into the cleared mammary fat pads of nude mice confirmed that this defect in ductal morphogenesis was intrinsic to the epithelium. When treated with estrogen/progesterone (E+P) to simulate pregnancy, C/EBP␤ −/− mammary glands displayed only limited lobuloalveolar development and ductal side branching. Primary mammary epithelial cells obtained from E+P-treated C/EBP␤ −/− mice that were cultured on extracellular matrix gels did not functionally differentiate in response to lactogenic hormones despite their organization into three-dimensional structures. Expression of ␤-casein protein was inhibited 85%-100% and whey acidic protein (WAP) was undetectable. In contrast, no detectable alterations in mammary development or ␤-casein expression were observed in mammary outgrowths derived from newborn C/EBP␣ −/− mammary epithelium transplanted into the cleared mammary fat pads of syngeneic hosts. These results demonstrate that C/EBP␤, but not C/EBP␣, is required for ductal morphogenesis, lobuloalveolar development, and functional differentiation of mammary epithelial cells.

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Null mutation of the prolactin receptor gene produces multiple reproductive defects in the mouse.

Cited by 711 publications

References 79 publications

Divergent roles of STAT1 and STAT5 in malignancy as revealed by gene disruptions in mice

Divergent roles of STAT1 and STAT5 in malignancy as revealed by gene disruptions in mice

Prolactin Is Not Required for the Development of Severe Chronic Experimental Autoimmune Encephalomyelitis

C/EBPβ, but not C/EBPα, is essential for ductal morphogenesis, lobuloalveolar proliferation, and functional differentiation in the mouse mammary gland

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