Hypoxia-induced energy stress regulates mRNA translation and cell growth.

By Liping Liu, T. Cash, Russell G. Jones, B. Keith, Craig B. Thompson, M. C. Simon. Molecules and Cells, 2006

631 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/21b6649481cd7e27625bc949b4fb7e2a55745665

How researchers see this paper

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

In Cancer Research

1. C. V. Dang
2. G. Semenza
3. Ralph J. Deberardinis
4. David M. Sabatini
5. Craig B. Thompson
6. Ping Gao
7. M. C. Simon
8. M. V. Vander Heiden

In Molecular Biology

1. David M. Sabatini
2. C. V. Dang
3. Ralph J. Deberardinis
4. R. Shaw
5. Craig B. Thompson
6. M. Laplante
7. G. Semenza
8. B. Manning

Citations in the corpus

• ER stress: Autophagy induction, inhibition and selection (2015, background): “Hypoxia stimulates extensive downregulation of protein synthesis through activation of the EIF2AK3-EIF2S1-ATF4 and AMPK-MTORC1 pathways.(158,159) Likewise, autophagy can also be triggered under hypoxic conditions, which can be attributed to hypoxia-induced Ca2C influx and activation of CAMK1 (calciu”
• AMPK is a negative regulator of the Warburg Effect and suppresses tumor growth in vivo (2012, background): “Consistent with past work (Inoki et al., 2003; Liu et al., 2006; Shaw et al., 2004a), we find that AMPK functions to downregulate TORC1 activity specifically under conditions of energetic stress, when it is desirable to suppress ATP-consuming processes such as mRNA translation.”
• Wound healing essentials: Let there be oxygen (2009, background): “Hypoxia causes ER stress, which in turn inhibits eIF2a.(185) Wound healing requires protein synthesis.”
• LKB1 and AMPK control of mTOR signalling and growth (2009, background): “…AMPK directly phosphorylates the TSC2 tumour suppressor on conserved serine sites distinct from those targeted by other kinases, which constitutes one mechanism by which glucose and oxygen control mTORC1 activation (Inoki et al. 2003, Corredetti et al. 2004, Shaw et al. 2004b, Liu et al. 2006).”
• Connecting endoplasmic reticulum stress to autophagy by unfolded protein response and calcium (2007, neutral): “In addition to ER stress, hypoxia also activates the PERKeIF2a-ATF4 and AMPK-mTORC1 pathways.(45,46) It is still unknown whether hypoxia also triggers autophagy, if so the”
• The TSC1-TSC2 complex: a molecular switchboard controlling cell growth. (2008, background): “Therefore hypoxia can inhibit mTORC1 through AMPK-mediated phosphorylation and activation of the TSC1–TSC2 complex [104].”
• AMPK phosphorylation of raptor mediates a metabolic checkpoint. (2008, background): “metics (Inoki et al., 2003; Corradetti et al., 2004; Shaw et al., 2004a, 2004b; Jones et al., 2005; Liu et al., 2006; Buzzai et al., 2007; Lee et al., 2007a).”
• Targeting hypoxia in cancer therapy (2011, background): “and through increased AMP-activated protein kinase (AMPK) activity under hypoxi”
• The mTOR Signalling Pathway in Human Cancer (2012, background): “AMPK/TSC2/Rheb pathway is activated at low oxygen levels, resulting in mTORC1 inhibition [75].”