Lesson plan
PAK1
Serine/threonine-protein kinase PAK 1 is an enzyme that in humans is encoded by the PAK1 gene. PAK1 is one of six members of the PAK family of serine/threonine kinases which are broadly divided into group I (PAK1, PAK2 and PAK3) and group II (PAK4, PAK6 and PAK5/7). The PAKs are evolutionarily conserved. PAK1 localizes in distinct sub-cellular domains in the cytoplasm and nucleus. PAK1 regulates cytoskeleton remodeling, phenotypic signaling and gene expression, and affects a wide variety of cellular processes such as directional motility, invasion, metastasis, growth, cell cycle progression, angiogenesis. PAK1-signaling dependent cellular functions regulate both physiologic and disease processes, including cancer, as PAK1 is widely overexpressed and hyperstimulated in human cancer, at-large. An activating point variant, c.1429G>T p.(Ala477Ser) (A477S), was reported in PAK1 in a patient with acute myeloid leukemia (AML). The variant was absent at diagnosis but detected at relapse, and functional studies showed that A477S increased PAK1 activation and promoted chemotherapy resistance.
Article summary
Serine/threonine-protein kinase PAK 1 is an enzyme that in humans is encoded by the PAK1 gene. PAK1 is one of six members of the PAK family of serine/threonine kinases which are broadly divided into group I (PAK1, PAK2 and PAK3) and group II (PAK4, PAK6 and PAK5/7). The PAKs are evolutionarily conserved. PAK1 localizes in distinct sub-cellular domains in the cytoplasm and nucleus. PAK1 regulates cytoskeleton remodeling, phenotypic signaling and gene expression, and affects a wide variety of cellular processes such as directional motility, invasion, metastasis, growth, cell cycle progression, angiogenesis. PAK1-signaling dependent cellular functions regulate both physiologic and disease processes, including cancer, as PAK1 is widely overexpressed and hyperstimulated in human cancer, at-large. An activating point variant, c.1429G>T p.(Ala477Ser) (A477S), was reported in PAK1 in a patient with acute myeloid leukemia (AML). The variant was absent at diagnosis but detected at relapse, and functional studies showed that A477S increased PAK1 activation and promoted chemotherapy resistance.
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Discussion questions
- Summarise the article in your own words. Which single claim would you verify first, and why?
- Which claim in this article is most likely to be revised as the sources update? How would you check its current status?
- If two sources disagreed about one of these facts, what would you need in order to trust one over the other?
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