Response Gene to Complement 32, a Novel Regulator for Transforming Growth Factor-β-induced Smooth Muscle Differentiation of Neural Crest Cells

Li, Fengmin; Luo, Zhiwei; Huang, Wenyan; Lu, Quansheng; Wilcox, Christopher S.; José, Pedro A.; Chen, Shiyou

doi:10.1074/jbc.c600225200

Cited by 47 publications

(62 citation statements)

References 56 publications

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“…Recently CNh1 was reported to play a major role in the stabilization of actin stress fibers, and the expression of CNh1 was up-regulated by the treatment with transforming growth factor (TGF)-β (Dykes and Wright 2007;Li et al 2007). The involvement of TGF-β in the interaction between Rho and CNh1 (Chen et al 2006) directs our study to TGF-β .…”

Section: Discussionmentioning

confidence: 99%

Tail-Suspended Mice Lacking Calponin H1 Experience Decreased Bone Loss

Yotsumoto¹,

Takeoka

Yokoyama

2010

Tohoku J. Exp. Med.

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Section: Discussionmentioning

confidence: 99%

Tail-Suspended Mice Lacking Calponin H1 Experience Decreased Bone Loss

Yotsumoto¹,

Takeoka

Yokoyama

2010

Tohoku J. Exp. Med.

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“…The primer sequences were as follows: Myocd, ACC CAT GGA CTC TGC CTA TG (forward) and AGG GGT ATT GCT CAG TGG TG (reverse); Nkx2.5, CAT TTT ACC CGG GAG CCT AC (forward) and GAC AGG TAC CGC TGT TGC TT (reverse). The primers used for SMC markers were described previously (22,31).…”

Section: Methodsmentioning

confidence: 99%

Smad3-mediated Myocardin Silencing

Xie

Miano

et al. 2011

Journal of Biological Chemistry

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“…These include angiogenesis, invasion and metastasis, suppression of antitumor CD8 + T-cells (77), and epithelial-to-mesenchymal transition (EMT) in numerous tumor types (77). Intriguingly, one of the downstream targets of TGF-β seems to be RGC-32, which has also been shown to regulate EMT (80,81). Not only has RGC-32 been implicated in control of the cell cycle and cancer (58-60) but it also shows upstream control by complement proteins, similar to TGF-β.…”

Section: Complement Sustains Tumorigenesismentioning

confidence: 99%

Cancer and the Complement Cascade

Rutkowski

Sughrue

Kane

et al. 2010

Molecular Cancer Research

229

249

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Despite significant research on the role of inflammation and immunosurveillance in the immunologic microenvironment of tumors, little attention has been given to the oncogenic capabilities of the complement cascade. The recent finding that complement may contribute to tumor growth suggests an insidious relationship between complement and cancer, especially in light of evidence that complement facilitates cellular proliferation and regeneration. We address the hypothesis that complement proteins promote carcinogenesis and suggest mechanisms by which complement can drive the fundamental features of cancer. Evidence shows that this diverse family of innate immune proteins facilitates dysregulation of mitogenic signaling pathways, sustained cellular proliferation, angiogenesis, insensitivity to apoptosis, invasion and migration, and escape from immunosurveillance. Given that the traditionally held functions for the complement system include innate immunity and cancer defense, our review suggests a new way of thinking about the role of complement proteins in neoplasia.

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Response Gene to Complement 32, a Novel Regulator for Transforming Growth Factor-β-induced Smooth Muscle Differentiation of Neural Crest Cells

Cited by 47 publications

References 56 publications

Tail-Suspended Mice Lacking Calponin H1 Experience Decreased Bone Loss

Tail-Suspended Mice Lacking Calponin H1 Experience Decreased Bone Loss

Smad3-mediated Myocardin Silencing

Cancer and the Complement Cascade

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