scholarly journals A Case of Pseudopregnancy in a Bitch

2021 ◽  
pp. 1-5
Author(s):  
C. S. Ukwueze ◽  
K. A. Raheem
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Associated Factors ◽  
Clinical Signs ◽  
Mammary Glands ◽  
Milk Secretion ◽  
Normal Range ◽  
Abdominal Palpation ◽  
Nesting Behaviour ◽  
Vaginal Cytology

A case of pseudopregnacy was presented to Veterinary Teaching Hospital, Michael Okpara University of Agriculture Umudike, Nigeria. Eighteen (18) months old bitch weighing 15kg was presentedclinical signs suspected to be pseudopregnacy, which was observed four weeks after the bitch came on heat (estrus). The clinical signs observed were restlessness, anorexia, aggression, nesting behaviour and licking of mammary gland. On clinical examination it was observed that bitch had enlarged mammary glands and milk secretion. The physiological parameters were found to be within the normal range.  Abdominal palpation, ultrasonography and vagina cytology were carried out to confirm pregnancy. Due to absence of foetuses on abdominal palpation and ultrasonography and presence of scanty epithelial cells in vaginal cytology, it was confirmed and concluded to be a case of pseudopregnancy. Causes, treatment and other associated factors with pseudopregnancy were further discussed.

scholarly journals Essential functions of p21-activated kinase 1 in morphogenesis and differentiation of mammary glands

2003 ◽  
Vol 161 (3) ◽  
pp. 583-592 ◽  
Author(s):  
Rui-An Wang ◽  
Ratna K. Vadlamudi ◽  
Rozita Bagheri-Yarmand ◽  
Iwan Beuvink ◽  
Nancy E. Hynes ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Mammary Gland Development ◽  
Mammary Epithelial Cells ◽  
Ectopic Expression ◽  
Functional Differentiation ◽  
Mammary Glands ◽  
Pregnancy And Lactation ◽  
P21 Activated Kinase ◽  
Gland Development

Although growth factors have been shown to influence mammary gland development, the nature of downstream effectors remains elusive. In this study, we show that the expression of p21-activated kinase (Pak)1, a serine/threonine protein kinase, is activated in mammary glands during pregnancy and lactation. By targeting an ectopic expression of a kinase-dead Pak1 mutant under the control of ovine β-lactoglobulin promoter, we found that the mammary glands of female mice expressing kinase-dead Pak1 transgene revealed incomplete lobuloalveolar development and impaired functional differentiation. The expression of whey acidic protein and β-casein and the amount of activated Stat5 in the nuclei of epithelial cells in transgenic mice were drastically reduced. Further analysis of the underlying mechanisms revealed that Pak1 stimulated β-casein promoter activity in normal mouse mammary epithelial cells and also cooperated with Stat5a. Pak1 directly interacted with and phosphorylated Stat5a at Ser 779, and both COOH-terminal deletion containing Ser 779 of Stat5a and the Ser 779 to Ala mutation completely prevented the ability of Pak1 to stimulate β-casein promoter. Mammary glands expressing inactive Pak1 exhibited a reduction of Stat5a Ser 779 phosphorylation. These findings suggest that Pak1 is required for alveolar morphogenesis and lactation function, and thus, identify novel functions of Pak1 in the mammary gland development.

scholarly journals Signal Transducer and Activator of Transcription 5a Mediates Mammary Ductal Branching and Proliferation in the Nulliparous Mouse

Endocrinology ◽  
2010 ◽  
Vol 151 (6) ◽  
pp. 2876-2885 ◽  
Author(s):  
Sarah J. Santos ◽  
Sandra Z. Haslam ◽  
Susan E. Conrad
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Mammary Gland Development ◽  
Kinase Inhibitor ◽  
Mammary Epithelial Cells ◽  
Nuclear Factor Κb ◽  
Mammary Glands ◽  
Mammary Epithelial ◽  
Signal Transducer ◽  
Gland Development

Signal transducer and activator of transcription (Stat)5a is a critical regulator of mammary gland development. Previous studies have focused on Stat5a’s role in the late pregnant and lactating gland, and although active Stat5a is detectable in mammary epithelial cells in virgin mice, little is known about its role during early mammary gland development. In this report, we compare mammary gland morphology in pubertal and adult nulliparous wild-type and Stat5a−/− mice. The Stat5a-null mammary glands exhibited defects in secondary and side branching, providing evidence that Stat5a regulates these processes. In addition, Stat5a−/− mammary glands displayed an attenuated proliferative response to pregnancy levels of estrogen plus progesterone (E+P), suggesting that it plays an important role in early pregnancy. Finally, we examined one potential mediator of Stat5a’s effects, receptor activator of nuclear factor-κB ligand (RANKL). Stat5a−/− mammary glands were defective in inducing RANKL in response to E+P treatment. In addition, regulation of several reported RANKL targets, including inhibitor of DNA binding 2 (Id2), cyclin D1, and the cyclin-dependent kinase inhibitor p21Waf1/Cip1, was altered in Stat5a−/− mammary cells, suggesting that one or more of these proteins mediate the effects of Stat5a in E+P-treated mammary epithelial cells.

Differential expression of the growth hormone receptor and growth hormone-binding protein in epithelia and stroma of the mouse mammary gland at various physiological stages

1999 ◽  
Vol 161 (1) ◽  
pp. 77-87 ◽  
Author(s):  
YN Ilkbahar ◽  
G Thordarson ◽  
IG Camarillo ◽  
F Talamantes
Keyword(s):  
Growth Hormone ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Growth Hormone Receptor ◽  
Mammary Epithelial Cells ◽  
Late Pregnancy ◽  
Mammary Glands ◽  
Mouse Mammary Gland ◽  
Mammary Epithelial ◽  
Mrna Levels

Increasing evidence suggests that GH is important in normal mammary gland development. To investigate this further, we studied the distribution and levels of growth hormone receptor (GHR) and GH-binding protein (GHBP) in the mouse mammary gland. At three weeks of age, the epithelial component of the right fourth inguinal mammary gland of female mice was removed. These animals were then either maintained as virgins until they were killed or they were mated. One group of the mated mice was killed on day 18 of pregnancy and the remaining mated animals were allowed to carry their pups until term and were killed on day 6 of lactation. At the time of death, both the intact left and the de-epithelialized right mammary glands were collected from all three groups. Some of the intact glands served as a source of epithelial cells, free of stroma. The mRNA levels for GHR and GHBP were measured in intact glands, epithelia-cleared fat pads, and isolated mammary epithelial cells. GHR and GHBP mRNAs were expressed in both the mammary epithelium and stroma. However, the levels of both GHR and GHBP mRNAs were significantly higher in the stroma as compared with the epithelium component. This increase for both mRNAs was from 3- to 12-fold at each physiological state examined. In the intact gland, both GHR and GHBP transcripts were highest in virgins, declined during late pregnancy, and the lowest levels were found in the lactating gland. GHBP and GHR protein concentrations were also assessed in intact glands and epithelia-free fat pads. Similar to the mRNAs, GHR and GHBP protein levels (means+/-s.e.m.) in intact glands were highest in virgin mice (0.891+/-0.15 pmoles/mg protein and 0.136+/-0.26 pmoles/mg protein respectively), declined during late pregnancy (0. 354+/-0.111 pmoles/mg protein and 0.178+/-0.039 pmoles/mg protein respectively), and were lowest during lactation (0.096+0.037 pmoles/mg protein and 0.017+0.006 pmoles/mg protein respectively). Immunocytochemistry utilizing specific antisera against mouse (m) GHR and mGHBP revealed that the two proteins are localized to both the stroma and parenchyma of mouse mammary glands, with similar patterns of immunostaining throughout the different physiological stages analyzed. GHR immunolocalized to the plasma membrane and cytosol of mammary epithelial cells and adipocytes, whereas the GHBP immunostaining was nuclear and cytosolic. In conclusion, we report here that GHR and GHBP mRNAs and proteins are expressed in both the epithelium and the stroma of mammary glands of virgin, pregnant, and lactating mice. In intact glands, GHR and GHBP proteins, as well as their transcripts are higher in abundance in virgin relative to lactating mice. At all physiological stages, GHR and GHBP mRNA levels are higher in the stroma compared with the parenchyma. These findings indicate that the actions of GH in the mammary gland are both direct through its binding to the epithelia, and indirect by binding to the stroma and stimulation of IGF-I production which, in turn, affects mammary epithelial development.

EFFECT OF SUCKLING AND OF EXTEROCEPTIVE STIMULATION UPON PROLACTIN RELEASE IN THE RAT DURING LATE LACTATION

1972 ◽  
Vol 52 (1) ◽  
pp. 11-22 ◽  
Author(s):  
F. MENA ◽  
C. E. GROSVENOR
Keyword(s):  
Mammary Gland ◽  
Post Partum ◽  
Mammary Glands ◽  
The Other ◽  
Male Rats ◽  
Milk Secretion ◽  
Suckling Period ◽  
Prolactin Release ◽  
Other Hand ◽  
Rat Pituitary

SUMMARY The results of experiments in which the prolactin in the primiparous rat pituitary was bioassayed suggested that the failure of suckling to release prolactin after 8 h of non-suckling on day 21 post-partum was due to the fact that prolactin had been discharged from the pituitary during the 8-h non-suckling period, presumably by exteroceptive signals emanating from the general environment of the animal room. This was substantiated in other experiments in which prolactin release was assessed indirectly through its stimulatory effects upon milk secretion. In these experiments, the mammary glands of rats maintained continuously in the animal room filled faster on day 21 after complete emptying of the glands by exogenous oxytocin, than did either rats on day 14 post-partum maintained continuously in the animal room or rats isolated in a room without other rats on day 21 post-partum. The glands of the latter two groups of rats could be stimulated to fill faster provided prolactin was injected 4 h before the initial emptying of the glands. The exteroceptive stimuli in the animal room environment that stimulated the release of prolactin in the 21-day post-partum rat apparently emanated at least in part from other lactating rats and/or their litters, since faster mammary gland refilling occurred in isolated 21 day post-partum rats when they were exposed to the presence of lactating rats with their litters for 30 min halfway through the 8-h non-suckling period which preceded the initial emptying of the gland. Exposure to male rats, on the other hand, was totally ineffective. A release of prolactin occurred in response to animal room environmental stimuli in the day 14 primiparous rat provided 13–14 day old foster pups were inserted in place of the mother's own pups on day 7. Thus, the rapidly changing characteristics of the pups from 14 to 21 days of age in some manner is involved in the increasing responsiveness of the exteroceptive mechanism for prolactin release which occurs from day 14 to day 21 post-partum.

scholarly journals Hyperthyroidism and production of precocious involution in the mammary glands of lactating rats

Reproduction ◽  
2002 ◽  
pp. 691-702 ◽  
Author(s):  
SM Varas ◽  
EM Munoz ◽  
MB Hapon ◽  
CI Aguilera Merlo ◽  
MS Gimenez ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Mammary Gland ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Binding Sites ◽  
Mammary Glands ◽  
Insulin Like Growth Factor ◽  
Mammary Involution ◽  
Igf I ◽  
Mammary Gland Epithelial Cells

This study investigated the influence of chronic hyperthyroidism on mammary function in lactating rats and the effects on their pups. Thyroxine-treated (10 microg per 100 g body weight per day; hyperthyroid (HT)) or vehicle-treated rats were mated 2 weeks after the start of treatment and killed with their litters on days 7, 14 and 21 of lactation. Serum concentrations of triiodothyronine (T(3)) and tetraiodothyronine (T(4)) increased in thyroxine-treated rats. In HT mothers, serum prolactin decreased on day 7 and day 14 of lactation, whereas insulin-like growth factor I (IGF-I) and progesterone concentrations decreased, and corticosterone increased on day 7 of lactation. In HT pups, T(4) concentration increased on day 7 and day 14 of lactation, whereas T(3) increased only on day 14 of lactation, and growth hormone increased on day 7 of lactation. Mammary prolactin binding sites did not vary, but there was an increase in the binding sites in the liver on day 14 of lactation in thyroxine-treated rats. In an acute suckling experiment, thyroxine-treated rats released less oxytocin, growth hormone and prolactin and excreted less milk than did control rats. Mammary casein, lactose and total lipid concentrations in thyroxine-treated rats were similar to those of control rats on day 14 of lactation. Histological studies of the mammary glands showed an increased proportion of alveoli showing reduced or no lumina and cells with condensed nuclei on day 14 and day 21 of lactation; the TdT-mediated dUTP nick-end labelling (TUNEL) test revealed an increase in apoptosis in alveolar cells on day 21 of lactation in thyroxine-treated rats. Expression of SGP-2, a gene expressed during mammary involution, increased in thyroxine-treated rats on day 14 and day 21 of lactation, whereas expression of insulin-like growth factor binding protein 5, a proapoptotic signal, was unchanged. Bcl-2, which promotes survival of mammary gland epithelial cells was unchanged, whereas expression of IGF-I, which also promotes survival of mammary gland epithelial cells, increased on day 21 of lactation in thyroxine-treated rats. These results indicate that thyroxine treatment produces some milk stasis as a result of impairments in suckling induced release of oxytocin that may initiate the first stage of mammary involution, increasing apoptosis in a gland that is otherwise actively producing and secreting milk.

scholarly journals Memoirs: The Growth-Changes in the Mammary Apparatus of Dasyurus and the Relation of the Corpora Lutea thereto

1911 ◽  
Vol s2-57 (226) ◽  
pp. 187-234
Author(s):  
CHAS. H. O'DONOGHUE
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Corpus Luteum ◽  
Secretory Activity ◽  
Sweat Glands ◽  
Corpora Lutea ◽  
Milk Secretion ◽  
Mammary Gland Tissue ◽  
Gland Tissue ◽  
Large Growth

Formation of the Gland.--(1) The teat anlagen arise from a proliferation of the cells of the Malpighian layer of the epidermis. (2) The mammary gland anlage arises as a solid cellular outgrowth from the follicles of especially strong hairs on the primitive teat anlage. (3) The hairs ou the teat anlage are equal in number to the main milk-ducts in the adult teat. (4) The proximal solid part of the mammary gland outgrowth gives rise to the main milk-duct and the distal, hollow branches to the mammary tubules of the adult. The Adult Gland.--(1) The fully grown gland in repose consists of six main ducts, with a lining epithelium several cells deep, opening on the teat. The ducts lead down into a large number of ramified twisted tubules whose walls are two cells thick. (2) It is the seat of continuous, but very slow, secretory activity. Changes prior to Ovulation.--There is an increase in the size and activity of both the sebaceous and sweat-glnnds of the pouch area, but very little, if any, growth in the mammary gland. Changes during Pregnancy.--(1) There is a large increase of mammary gland tissue at this period, resting upon the initotic division of its epithelial cells, and resulting in the formation of a great number of true alveoli with single-layered walls and a secretion of lymph. (2) The sebaceous and sweat-glands of the pouch area also hypertrophy and become active, the secretion of the latter appearing as drops of a reddish fluid. (3) The greater part (practically the whole) of the growth in actual gland-tissue occurs before the attachment of the embryo. Changes after Parturition.--(1) The secretion of milk does not commence until about twenty-four hours after the birth of the young. (2) Such secretion results from a purely secretory activity of the cells of the glandular epithelium, and is not connected with necrobiosis of either cytoplasm or nucleus. Changes wheu Ovulation is not succeeded by Pregnancy.--(1) A large growth of the mammary gland-tissue occurs, due to the mitotic divisions of its epithelial cells, and it results in the formation of true alveoli wioh single-layered walls. A substance which resembles milk is secreted in small quantities in these alveoli. (2) The sebaceous and sweat-glands of the pouch area hypertrophy and become active. (3) The above changes are very similar to, indeed indistinguishable from, those taking place during pregnancy. Stimulus causing the growth of the Mammary Glands.--(1) The stimulus causing the hypertrophy of the mammary gland at any time is not a nervous one, but of the nature of an internal secretion carried by the blood. (2) The seat of origin of the stimulus produciug this growth at, puberty, during heat, in virgins that have given milk, and in Dasyurus after ovulation not succeeded by pregnancy is neither in the foetus nor in the placenta. (3) The presence of a functional ovary is necessary for the growth of the gland at all times. (4) The Corpus luteum is a ductless g-land producing an internal secretion which is responsible for the attachment of the embryo to the wall of the uterus. (5) (A) In Dasyurus, in the non-pregnant as well as in the pregnant animals, the formation and growth of the corpora lutea are intimately connected with the growth of the mammary gland. In the non-pregnant animals the secretion of the corpora lutea appears to be the only assignable cause of the growth of the gland. (B) In the rabbit, (a) the presence of an ovary (with Corpora lutea) is necessary for the growth of the mammary gland; (b) the growth of the mammary gland follows on the experimentally induced production of Corpora lutea. The general conclusion supported by the above evidence is that the Corpus luteum is a ductless gland producing a secretion which is the inciting cause of the growth of the mammary gland. Cause of Milk Secretion.--There is at present no satisfactory theory of the causation of milk secretion. That of the removal by parturition of an inhibitory stimulus originating in the placenta or foetus does not meet all cases.

Differential regulation of GLUT1 and GLUT8 expression by hypoxia in mammary epithelial cells

2014 ◽  
Vol 307 (3) ◽  
pp. R237-R247 ◽  
Author(s):  
Yong Shao ◽  
Theresa L. Wellman ◽  
Karen M. Lounsbury ◽  
Feng-Qi Zhao
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Glucose Uptake ◽  
Mammary Epithelial Cells ◽  
Physiological Mechanism ◽  
Glucose Transporters ◽  
Mammary Glands ◽  
Mammary Development ◽  
Mammary Epithelial ◽  
Early Lactation

Glucose is a major substrate for milk synthesis and is taken up from the blood by mammary epithelial cells (MECs) through facilitative glucose transporters (GLUTs). The expression levels of GLUT1 and GLUT8 are upregulated dramatically in the mammary gland from late pregnancy through early lactation stages. This study aimed to test the hypothesis that this increase in GLUT1 and GLUT8 expression involves hypoxia signaling through hypoxia inducible factor-1α (HIF-1α) in MECs. Mouse mammary glands showed significantly more hypoxia in midpregnancy through early lactation stages compared with in the virgin stage, as stained by the hypoxia marker pimonidazole HCl. Treatment with hypoxia (2% O2) significantly stimulated glucose uptake and GLUT1 mRNA and protein expression, but decreased GLUT8 mRNA expression in bovine MECs. In MECs, hypoxia also increased the levels of HIF-1α protein in the nuclei, and siRNA against HIF-1α completely abolished the hypoxia-induced upregulation of GLUT1, while having no effect on GLUT8 expression. A 5′-RCGTG-3′ core HIF-1α binding sequence was identified 3.7 kb upstream of the bovine GLUT1 gene, and HIF-1α binding to this site was increased during hypoxia. In conclusion, the mammary glands in pregnant and lactating animals are hypoxic, and MECs respond to this hypoxia by increasing GLUT1 expression and glucose uptake through a HIF-1α-dependent mechanism. GLUT8 expression, however, is negatively regulated by hypoxia through a HIF-1α-independent pathway. The regulation of glucose transporters through hypoxia-mediated gene transcription in the mammary gland may provide an important physiological mechanism for MECs to meet the metabolic demands of mammary development and lactation.

Effects of chlorpromazine on mammary glands of rats

1960 ◽  
Vol 199 (6) ◽  
pp. 1073-1076 ◽  
Author(s):  
P. K. Talwalker ◽  
J. Meites ◽  
C. S. Nicoll ◽  
T. F. Hopkins
Keyword(s):  
Body Weight ◽  
Mammary Gland ◽  
Anterior Pituitary ◽  
Post Partum ◽  
Mammary Glands ◽  
Adrenal Weight ◽  
Milk Secretion ◽  
Estradiol Treatment ◽  
Litter Removal ◽  
Thymus Weight

The effects of chlorpromazine were determined on mammary growth and initiation of milk secretion in virgin rats, and on maintenance of mammary structure and secretion in postpartum rats after litter removal. When chlorpromazine was administered in doses of 5 or 15 mg/kg body weight for 5 days, only the higher dose was effective in inducing lobulo-alveolar growth and initiating milk secretion in rats initially primed with 10 µg estradiol daily for 10 days. The higher dose of chlorpromazine also maintained mammary lobulo-alveolar structure and secretion in post-partum rats for 10 days after litter removal. Chlorpromazine produced a significant increase in adrenal weight and decrease in thymus weight, indicating adrenal stimulation. In estrogen-primed rats neither prolactin nor ACTH alone could initiate mammary secretion; however they were effective when given in combination. The present data indicate that chlorpromazine promotes the secretion of both prolactin and ACTH. Hypophysectomy following estradiol treatment prevented chlorpromazine from initiating mammary secretion, showing that its effects are mediated through the anterior pituitary and not directly on the mammary gland.

scholarly journals Scribble promotes alveologenesis in the pregnant mammary gland for milk production

Reproduction ◽  
2020 ◽  
Vol 159 (6) ◽  
pp. 719-731
Author(s):  
Shizu Aikawa ◽  
Jia Yuan ◽  
Amanda Dewar ◽  
Xiaofei Sun ◽  
Sudhansu K Dey
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Milk Production ◽  
Critical Role ◽  
Cell Lineage ◽  
Mammary Glands ◽  
Transcriptional Factor ◽  
Alveolar Cells ◽  
Terminal End Bud ◽  
Luminal Epithelial Cells

Mammary glands are comprised of ducts and terminal lobules that form tree-like structures. Luminal epithelial cells in these lobules undergo differentiation into alveolar cells in pregnancy to support milk production. This study reveals that Scribble (SCRIB), a scaffold protein expressed in progesterone receptor (PGR)-positive cells, plays a critical role in mammary gland alveologenesis in mice. We conditionally deleted Scrib using a Pgr-Cre driver. PGR is heterogeneously expressed throughout the luminal epithelium. Scrib loss in mammary glands by Pgr-Cre (Scribf/fPgrCre/+) shows inefficient alveologenesis and terminal end bud (TEB)-like morphology during pregnancy, resulting in poor milk production and subsequent death of pups after delivery. The differentiation of PGR-positive epithelial cells into Elf5-expressing alveolar cells is defective in Scribf/fPgrCre/+ mice. These changes are reflected in reduced activation of JAK2 and PAK1, resulting in downregulation of pSTAT5, a critical transcriptional factor for alveologenesis. These results provide evidence that SCRIB impacts PGR-positive cell lineage during alveologenesis, which impacts milk production and the health of offspring.

scholarly journals ZnT4 provides zinc to zinc-dependent proteins in the trans-Golgi network critical for cell function and Zn export in mammary epithelial cells

2012 ◽  
Vol 303 (3) ◽  
pp. C291-C297 ◽  
Author(s):  
Nicholas H. McCormick ◽  
Shannon L. Kelleher
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Cell Membrane ◽  
Cell Function ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Milk Secretion ◽  
Trans Golgi Network ◽  
Dependent Protein ◽  
Golgi Network

Zinc (Zn) transporter 4 (ZnT4) plays a key role in mammary gland Zn metabolism. A mutation in ZnT4 ( SLC30A4) that targets the protein for degradation is responsible for the “lethal milk” ( lm/lm) mouse phenotype. ZnT4 protein is only detected in the secreting mammary gland, and lm/lm mice have ∼35% less Zn in milk, decreased mammary gland size, and decreased milk secretion. However, the precise contribution of ZnT4 is unknown. We used cultured mouse mammary epithelial cells (HC11) and determined that ZnT4 was localized to the trans-Golgi network (TGN) and cell membrane and transported Zn from the cytoplasm. ZnT4-mediated Zn import into the TGN directly contributed to labile Zn accumulation as ZnT4 overexpression increased FluoZin3 fluorescence. Moreover, ZnT4 provided Zn for metallation of galactosyltransferase, a Zn-dependent protein localized within the TGN that is critical for milk secretion, and carbonic anhydrase VI, a Zn-dependent protein secreted from the TGN into milk. We further noted that ZnT4 relocalized to the cell membrane in response to Zn. Together these studies demonstrated that ZnT4 transports Zn into the TGN, which is critical for key secretory functions of the mammary cell.

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