Vascular endothelial growth factor–induced elimination of the type 1 interferon receptor is required for efficient angiogenesis

Zheng, Hui; Qian, Juan; Carbone, Christopher J.; Leu, N. Adrian; Baker, Darren P.; Fuchs, Serge Y.

doi:10.1182/blood-2011-06-359745

Cited by 66 publications

(66 citation statements)

References 23 publications

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“…IFN inhibits angiogenesis by acting directly on tumor cells and on lymphocyte-induced vascular responses (91,92). Interestingly, VEGF needs to downregulate type I IFN receptor expression in order to induce efficient angiogenesis (93). An additional explanation for greatly increased growth of several tumors including MC38 in Ifnb −/− or Ifnar1 −/− mice has been ascribed to Gr1 + neutrophils that promote tumor angiogenesis and tumor growth in both Ifnb −/− and WT mice and are hyperactivated in the TME of Ifnb −/− mice (66).…”

Section: Discussionmentioning

confidence: 99%

Interferon-dependent IL-10 production by Tregs limits tumor Th17 inflammation

Stewart¹,

Metheny²,

Iida³

et al. 2013

J. Clin. Invest.

145

104

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Section: Discussionmentioning

confidence: 99%

Interferon-dependent IL-10 production by Tregs limits tumor Th17 inflammation

Stewart¹,

Metheny²,

Iida³

et al. 2013

J. Clin. Invest.

145

104

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“…Notably, endothelial cells respond to VEGF by upregulating the UPR, which supports VEGF-mediated angiogenesis [70]. In addition, anti-angiogenic Type I interferon signaling is inactivated via both VEGF and UPR-induced degradation of the interferon receptor [71, 72]. HIF1α heterodimerization with sXBP1, which has been demonstrated in breast cancer cells, exemplifies cooperation between the UPR and hypoxia, an activity that was implicated in maintenance of triple-negative breast cancer (TNBC).…”

Section: The Upr Link With Mitochondrial Functionmentioning

confidence: 99%

UPR, autophagy, and mitochondria crosstalk underlies the ER stress response

Senft

Ronai

2015

Trends in Biochemical Sciences

895

687

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Cellular stress, induced by external or internal cues, activates several well-orchestrated processes aimed at either restoring cellular homeostasis or committing to cell death. Those processes include the unfolded protein response (UPR), autophagy, hypoxia, and mitochondrial function, which are part of the global ER stress (ERS) response. When one of the ERS elements is impaired, as often occurs under pathological conditions, overall cellular homeostasis may be perturbed. Further, activation of the UPR could trigger changes in mitochondrial function or autophagy, which could modulate the UPR, exemplifying cross-talk processes. Among the numerous factors that control the magnitude or duration of these processes are ubiquitin ligases, which govern overall cellular stress outcomes. Here we summarize crosstalk among fundamental processes governing ERS responses.

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“…This cross-linking protein is critical for SAC regulation (SharifNaeini et al, 2009;Nilius and Honore, 2013;Peyronnet et al, 2013). TRPP1 is involved in angiogenesis via modulation of VEGF and type-1 interferons (IFNs), including IFNa/b, and plays a role in lithium-induced neuritogenesis (Italia et al, 2011;Zheng et al, 2011).…”

Section: F Polycystic Transient Receptor Potential Subfamilymentioning

confidence: 99%