Serine phosphorylation of STATs

By T. Decker, P. Kovarik. Oncogene, 2000

925 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/bd15e9bf01fb8929730dca612b75111742be95a3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. M. Laplante
2. David M. Sabatini
3. R. Jove
4. D. Levy
5. R. A. Saxton
6. Michael N. Hall
7. K. Guan
8. L. Bar-Peled

In Oncology

1. R. Jove
2. D. Levy
3. David M. Sabatini
4. M. Laplante
5. Chien-Kuo Lee
6. Jacqueline F. Bromberg

Citations in the corpus

• What does Stat3 do? (2002, background): “The identity of the serine kinase for Stat3 is somewhat controversial, most likely because different activation signals lead to serine phosphorylation by any of several kinases, including ERK1, ERK2, p38, JNK, and an H-7–sensitive kinase (14).”
• The crucial role of protein phosphorylation in cell signaling and its use as targeted therapy (Review) (2017, neutral): “This complex phosphorylates Stat1, leading to its dimerization and nuclear translocation, where it regulates gene transcription (62-65).”
• Regulation of mTORC1 and its impact on gene expression at a glance (2013, background): “Additionally, STAT3 can be phosphorylated by numerous kinases on Ser727, a site that promotes its transcriptional activity (reviewed by Decker and Kovarik, 2000).”
• STAT proteins: From normal control of cellular events to tumorigenesis (2003, background): “Such modifications include not only ubiquitination, which targets some STATs for proteolysis (Wang et al., 2000), but also serine phosphorylation (Decker and Kovarik, 2000), and potentially acetylation, arginine methylation, and SUMO-ylation (Sachdev et al., 2001), all potential mechanisms for…”
• STAT proteins: novel molecular targets for cancer drug discovery (2000, background): “Because of the key role of serine phosphorylation for maximal transcriptional activity of some STATs (for review, see Decker and Kovarik, 2000), it is predicted that inhibition of this modi®cation would be su cient to impair STAT activity.”
• Mechanisms of estrogen receptor signaling: convergence of genomic and nongenomic actions on target genes. (2005, background): “It has been suggested that additional serine phosphorylation modulates the maximal transcriptional activity of STATs (77).”