prlr - Synonyms for prlr | Synonyms Of prlr

Examples of "prlr"
The PRLR has been found to be essential for lobuloalveolar maturation of the mammary glands during pregnancy, as evidenced by the fact that PRLR knockout mice show severely impaired development of lobuloalveolar structures.
PHYHIPL; PRLR; PRODH2; PTPRB; PTPRC; PTPRD; PTPRF; PTPRG;
The prolactin receptor (PRLR)—encoded by a gene on chromosome 5p13-14—interacts with prolactin as a transmembrane receptor. Thus it contains an extracellular region that binds prolactin, a transmembrane region, and a cytoplasmatic region. The PRLR also binds and is activated by growth hormone (GH) and human placental lactogen (hPL) in addition to prolactin.
The PRLR is a cytokine receptor, and second messenger cascades include the JAK-STAT pathway, JAK-RUSH pathway, Ras-Raf-MAPK, and PI3K/AKT/mTOR pathway.
Upon parturition (childbirth), estrogen and progesterone rapidly drop to very low levels, with progesterone levels being undetectable, while prolactin levels remain elevated. As estrogen and progesterone block prolactin-induced lactogenesis, by suppressing prolactin receptor (PRLR) expression in breast tissue, specifically, their sudden absence results in the commencement of milk production and lactation by prolactin. Expression of the PRLR in breast tissue may increase by as much as 20-fold when estrogen and progesterone levels drop upon childbirth. With suckling from the infant, prolactin and oxytocin are secreted and mediate milk production and letdown, respectively. Prolactin suppresses the secretion of LH and FSH, which in turn results in continued low levels of estrogen and progesterone, and temporary amenorrhea (absence of menstrual cycles) occurs. In the absence of regular, episodic suckling, which keeps prolactin concentrations high, levels of prolactin will quickly drop, the menstrual cycle will resume and hence normal estrogen and progesterone levels will return, and lactation will cease (that is, until next parturition, or until induced lactation (i.e., with a galactogogue), occurs).
During pregnancy, pronounced breast growth and maturation occurs in preparation of lactation and breastfeeding. Estrogen and progesterone levels increase dramatically, reaching levels by late pregnancy that are several hundred-fold higher than usual menstrual cycle levels. Estrogen and progesterone cause the secretion of high levels of prolactin from the anterior pituitary, which reach levels as high as 20 times greater than normal menstrual cycle levels. IGF-1 and IGF-2 levels also increase dramatically during pregnancy, due to secretion of placental growth hormone (PGH). Further ductal development, by estrogen, again in conjunction with GH/IGF-1, occurs during pregnancy. In addition, the concert of estrogen, progesterone (again specifically through PRB), prolactin, and other lactogens such as human placental lactogen (hPL) and PGH, in conjunction with GH/IGF-1, as well as insulin-like growth factor 2 (IGF-2), acting together, mediate the completion of lobuloalveolar development of the breasts during pregnancy. Both PR and prolactin receptor (PRLR) knockout mice fail to show lobuloalveolar development, and progesterone and prolactin have been found to be synergistic in mediating growth of alveoli, demonstrating the essential role of both of these hormones in this aspect of breast development. Growth hormone receptor (GHR) knockout mice also show greatly impaired lobuloalveolar development. In addition to their role in lobuloalveolar growth, prolactin and hPL act to increase the size of the nipple-areolar complex during pregnancy. By the end of the fourth month of pregnancy, at which time lobuloalveolar maturation is complete, the breasts are fully prepared for lactation and breastfeeding.