ATF4 is a substrate of RSK2 and an essential regulator of osteoblast biology; implication for Coffin-Lowry Syndrome.

By Xiangli Yang, Koichi Matsuda, P. Bialek, S. Jacquot, H. Masuoka, T. Schinke, Lingzhen Li, S. Brancorsini, Paolo Sassone-Corsi, T. Townes and 2 more. Cell, 2004

834 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/45242387df85d77febc8e2209178c16000c8ba0e

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Citations in the corpus

• Activation and Function of the MAPKs and Their Substrates, the MAPK-Activated Protein Kinases (2011, background): “Both c-Fos and ATF4 transcription factors have been proposed to be critical targets of RSK2 mediating its effects in osteoblasts (80, 413).”
• The GCN2‐ATF4 pathway is critical for tumour cell survival and proliferation in response to nutrient deprivation (2010, background): “ATF4 also appears to have multiple functions during development: ATF4 knockout mice exhibit abnormal lens formation, growth retardation, anemia and delayed bone development (Tanaka et al, 1998; Masuoka and Townes, 2002; Yang et al, 2004).”
• From acute ER stress to physiological roles of the Unfolded Protein Response (2006, background): “major ER stress markers, ATF4, has been reported to regulate the onset of osteoblast differentiation, type I collagen synthesis, osteoblast-specific gene expression, and osteoblast terminal differentiation.(95) Osteoblasts express high levels of ATF4 protein compared to most other tissues.”
• Lrp5 controls bone formation by inhibiting serotonin synthesis in the duodenum: an entero-bone endocrine axis (2008, background): “Removing one allele of Atf4, a CREB-related osteoblast-enriched transcription factor (Yang et al., 2004), from Lrp5+/− mice did not affect the bone phenotype of these latter mice arguing against a role for ATF4 in mediating serotonin signaling in osteoblasts (Figure 6A and S6).”
• Histone deacetylase 4 controls chondrocyte hypertrophy during skeletogenesis. (2004, background): “In contrast, bones that form through intramem- branous ossification, such as the clavicle, were unaf-important in osteoblast differentiation (Yang et al., 2004), (B) Top panel: COS cells were transfected with expression plasmids encoding Flag-epitope-tagged Runx2 deletion mutants (shown to the…”
• Development of the endochondral skeleton. (2013, background): “Misregulation of ATF4 activity has been linked with the skeletal abnormalities seen in human patients with Coffin–Lowry syndrome and neurofibromatosis type I (Yang et al. 2004; Elefteriou et al. 2006).”
• Regulation of osteoblast differentiation by transcription factors (2006, background): “Both ATF4 / mice and RSK2 / mice show disturbance in type I collagen production [Yang et al., 2004] (Fig.”
• The integrated stress response (2016, unknown): “Phosphorylation of ATF4 at S245 by ribosomal protein S6 kinase a-2 (RSK2) or S254 by protein kinase A (PKA) can enhance its transcriptional activity during osteoblast and osteoclast differentiation [107,159].”