ライフサイエンスコーパス: mammary epithelia

1 uggest a cell type-specific role for TP53 in mammary epithelia.

2 th conditional loss of murine p53 (Trp53) in mammary epithelia.

3 " prepared from Cav-1(-/-) MSFs on wild-type mammary epithelia.

4 ary to restore functional differentiation of mammary epithelia.

5 ks, compromises the self-renewal capacity of mammary epithelia.

6 trate, was mislocalized in mitotic Chk1(+/-) mammary epithelia.

7 G cells, which are derived from normal mouse mammary epithelia.

8 ry gland development and in cultured primary mammary epithelia.

9 d required localization within the nuclei of mammary epithelia.

10 brane domains in non-muscle cells, including mammary epithelia.

11 cated in the oncogenesis of the prostate and mammary epithelia.

12 n and that it is abundantly expressed in the mammary epithelia and brain.

13 This suggests a survival role for IRF-1 in mammary epithelia and demonstrates a novel role for IRF-

14 ivation promotes premalignant alterations in mammary epithelia and induces increased ERalpha expressi

15 that BMPR2 has tumor-suppressive function in mammary epithelia and microenvironment and that disrupti

16 formed in models that represent immortalized mammary epithelia and multiple subtypes of breast cancer

17 ator of proliferation and differentiation in mammary epithelia and represents a crucial prognostic in

18 factors are required for the survival of the mammary epithelia and what role these adipokines play in

19 expression is increased in Cav-1 (-/-) null mammary epithelia, and estrogen stimulation further enha

20 ediates prolactin-induced differentiation of mammary epithelia, and loss of Stat5 signaling in human

21 is the predominant SENP transcript in human mammary epithelia but is significantly reduced in precan

22 Thus, a Cav-1 deficiency profoundly affects mammary epithelia by modulating the activation state of

23 discovered that Cre-Lox ablation of Rac1 in mammary epithelia causes gross enlargement of the epithe

24 sion of an insulin receptor (IR) in a normal mammary epithelia] cell line causes insulin-dependent tr

25 Increased apoptosis occurred in the mammary epithelia, consistent with the inhibition of a W

26 Hyperproliferative mammary epithelia contained increased apoptotic cells, s

27 nsgenic mice deregulated for cyclin E in the mammary epithelia develop carcinoma, confirming that cyc

28 Differentiated mammary epithelia did not form in the combined absence o

29 we demonstrate that depletion of Scribble in mammary epithelia disrupts cell polarity, blocks three-d

30 Human ErbB-2 was expressed in the secretory mammary epithelia during pregnancy and lactation and exp

31 ) that disrupt the differentiation of normal mammary epithelia, expand stem and luminal progenitor ce

32 ave been noted in comparing the responses of mammary epithelia from nulliparous versus parous females

33 Transplantation of mammary epithelia from Wnt-4(-)/(-) mice shows that Wnt-

34 Within mammary epithelia, Gal-1 localized within nuclear Gemini

35 larization of early hyperplastic portions of mammary epithelia in NeuYD;MMTV-VEGF animals was associa

36 icting Par3 and aPKC to the apical region in mammary epithelia in vivo, and found that mammary morpho

37 Ac) epitopes, induces branching migration of mammary epithelia in vivo, ex vivo, and in 3D organotypi

38 anding how cell cycle is regulated in normal mammary epithelia is essential for deciphering defects o

39 Mammary epithelia lacking Elf5 exhibited downregulation

40 We show that in postnatal mammary epithelia, LBH is predominantly expressed in the

41 imals, low levels of transgene expression in mammary epithelia led to increased expression of endogen

42 Coexpression of EZH2(T416D) in mammary epithelia of HER2/Neu transgenic mice reprograms

43 function is an early event occurring in the mammary epithelia of midlactation mammary glands in whic

44 The mammary epithelia of MMTV betaTrcp1 mice proliferate mor

45 These phenotypes in the mammary epithelia of the transgenic mice are not depende

46 In both uterine and mammary epithelia of these mice, MMP-7 localization is a

47 develop mammary cancer due to expression in mammary epithelia of transforming growth factor alpha (T

48 he matrix metalloproteinase stromelysin-1 to mammary epithelia of transgenic mice resulted in reduced

49 testinal epithelium, unlike in epidermal and mammary epithelia, of mice does not result in decreased

50 First, we demonstrated that Cav-1(-/-) mammary epithelia overexpress two well-established ER co

51 We uncover a dual role for Rank in the mammary epithelia: Rank induces senescence and stemness,

52 studies indicate two distinct populations of mammary epithelia that express nestin: one expressing cy

53 imilar phenotypes were observed in Pten-null mammary epithelia that had been transplanted into wild-t

54 paB (RANK) pathway mediates the expansion of mammary epithelia that occurs during pregnancy, and acti

55 mary, overexpression of cyclin D1 may commit mammary epithelia to a tumor-prone phenotype in which co

56 101 seemed to increase the susceptibility of mammary epithelia toward malignant transformation.

57 sion of proteolytically active MMP3 in mouse mammary epithelia triggers supernumerary lateral branchi

58 otif containing protein 24 (TRIM24) in mouse mammary epithelia (Trim24(COE)) drives spontaneous devel

59 we show that ectopic Rank expression in the mammary epithelia unexpectedly delays tumor onset and re

60 ein interaction landscape of non-transformed mammary epithelia versus breast cancer cells in parallel

61 al cells affects the differentiated state of mammary epithelia via paracrine signaling.

62 pRb-deficient mammary epithelia were capable of functional differentia

63 Cav-1-/- mammary epithelia were hyperproliferative in vivo, with

64 PrlR- and Stat5-null mammary epithelia were transplanted into wild-type hosts

65 Primary cultures of Cav-1-deficient mammary epithelia will provide a valuable new model to s