The E3 ubiquitin ligase itch couples JNK activation to TNFalpha-induced cell death by inducing c-FLIP(L) turnover.

By Lufen Chang, H. Kamata, G. Solinas, Jun-Li Luo, S. Maeda, K. Venuprasad, Yun-Cai Liu, M. Karin. Cell, 2006

605 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/752e64583657a10f9455fe863ba9ce46c4a0718d

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. Ivan Dikic
2. A. Ashkenazi
3. Zhaoyu Jin
4. D. Komander
5. M. Karin
6. V. Bhoj
7. E. Wagner
8. A. Nebreda

In Molecular Biology

1. D. Komander
2. Ivan Dikic
3. E. Wagner
4. A. Nebreda
5. Zhaoyu Jin
6. D. Lawrence
7. Jennie Lill
8. Yun Li

Citations in the corpus

• Nuclear factor-κB in cancer development and progression (2006, background): “Decreased NF-κB activity and elevated JNK activity promote TNF-α-induced cell deat”
• Cullin3-based polyubiquitination and p62-dependent aggregation of caspase-8 mediate extrinsic apoptosis signaling. (2009, positive): “In TNFa signaling, JNK stimulation induces ITCH-dependent ubiquitination and proteasomal degradation of the apical caspase inhibitor FLIP, indirectly augmenting caspsae-8 activation (Chang et al., 2006).”
• Specific recognition of linear ubiquitin chains by NEMO is important for NF-kappaB activation. (2009, methodology): “…TNF-a under different conditions can mediate either cell survival or apoptosis, presumably via changes in the level of NF-kB and JNK activities (Chang et al., 2006), we next monitored TNF-a-induced cell death by evaluating the cleavage of caspase-3 and changes in chromatin condensation in MEFs…”
• Immunity, Inflammation, and Cancer (2010, neutral): “, 2004), c-FLIP seems to fulfill the same function in hepatocytes (Chang et al., 2006).”
• Signal integration by JNK and p38 MAPK pathways in cancer development (2009, background): “One pathway that has been suggested involves the E3 ubiquitin ligase ITCH , which degrades the caspase 8 inhibitor CASP8 and FADD-like apoptosis regulator ( CFLAR ; also known as FLIP) through JNK1 phosphorylation of ITC”
• Life and death by death receptors (2009, positive): “However, JNK-sustained activation mediates phosphorylation and activation of the E3 ubiquitin ligase Itch, which specifically ubiquitinates c-FLIP and promotes its proteasomal degradation, resulting in enhanced caspase 8 activation and apoptosis (137).”
• Ubiquitylation in innate and adaptive immunity (2009, background): “The degradation of c-FLIP is mediated by ITCH, a ubiquitin ligase whose activity is enhanced by JNK-catalysed phosphorylatio”
• Physiological functions of the HECT family of ubiquitin ligases (2009, background): “Moreover, Jnk protein activity also controls tumour necrosis factor-α (TNFα)-induced apoptosis through ITCH-mediated degradation of FLIP (also known as casper), an inhibitor of caspase 8-mediated apoptosis that is normally stimulated by NF-κ”