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- W134480872 abstract "Reproduction in mammals is controlled by the synthesis and secretion of GnRH released from specific neurons in the hypothalamus. GnRH stimulates the anterior pituitary to secrete LH and FSH, the primary hormones that regulate reproductive function. Upon binding of GnRH to its receptor, multiple signaling steps culminate in the activation of ERK. It is currently known that the magnitude and duration of ERK is dependent on positive and negative feedback. In L[beta]T2 cells, it is well established that GnRH acts as a positive regulator of ERK activation, while the dual specificity protein phosphatase DUSP-1 has been shown to mediate negative feedback and deactivation. We hypothesize that DUSP-1 differentially regulates activation of ERK based on cellular location. To determine if in response to GnRH DUSP-1 mediates ERK activation based on cellular location, two important mediators in LH gene expression, ELK and eIF4E, which exist in distinct cellular compartments, were examined to determine differential activation. In addition, nuclear and cytoplasmic fractions were collected to evaluate the relative activation of ERK in each and the activation and cellular location of DUSP-1. In addition, current literature shows sequence specific RNA-binding proteins that bind to target mRNA regulating their stability and translation. Hence, the regulation of DUSP-1 mRNA by HuR RNA-BP in response to GnRH was preliminarily examined through immunoprecipitation, nuclear and cytoplasmic fractionation, immunofluorescence, and ribosome fractionation. We conclude that in LBT2 cells DUSP-1 differentially regulates ERK activation based on cellular location and that HuR may be regulating the expression of DUSP-1." @default.
- W134480872 created "2016-06-24" @default.
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- W134480872 date "2009-01-01" @default.
- W134480872 modified "2023-09-27" @default.
- W134480872 title "Role and regulation of DUSP-1 in GnRH signaling" @default.
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