Abstract
Prolactin (PRL) and growth hormone (GH) act by way of their receptors as either hormones (systemically) or cytokines (locally). The Jak2/Stat5 pathway is the principal route by which PRL/GH activate target genes. The availability of knockout mice for each member of this signaling cascade has provided opportunities to understand their unique interactions. Jak2 is important in alternative signal transduction schema such as the MAP kinase and PI3K/Akt pathways. The putative Jak2/RUSH pathway is based on the fact that RUSH mediates the ability of PRL to augment progesterone-dependent gene transcription. New evidence shows that suppressors, regulators, and degraders control Jak2/Stat5. This review focuses on the most recent advances in the field of PRL/GH signal transduction.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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DNA-Binding Proteins / physiology
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Growth Hormone / physiology*
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Humans
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Janus Kinase 2
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Mice
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Milk Proteins
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Models, Biological
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Prolactin / physiology*
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Protein-Tyrosine Kinases / physiology
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Proto-Oncogene Proteins / physiology
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Receptors, Prolactin / chemistry
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Receptors, Prolactin / physiology
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Receptors, Somatotropin / chemistry
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Receptors, Somatotropin / physiology
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STAT5 Transcription Factor
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Signal Transduction
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Trans-Activators / physiology
Substances
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DNA-Binding Proteins
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Milk Proteins
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Proto-Oncogene Proteins
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Receptors, Prolactin
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Receptors, Somatotropin
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STAT5 Transcription Factor
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Trans-Activators
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Prolactin
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Growth Hormone
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Protein-Tyrosine Kinases
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JAK2 protein, human
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Jak2 protein, mouse
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Janus Kinase 2