Fanconi anemia protein complex is a novel target of the IKK signalsome

@article{Otsuki2002FanconiAP,
  title={Fanconi anemia protein complex is a novel target of the IKK signalsome},
  author={Tetsuya Otsuki and David B. Young and Dennis T. Sasaki and Matthew P. Pando and Jianwu Li and Anthony M. Manning and Merl F. Hoekstra and Maureen E. Hoatlin and Frank Mercurio and Johnson M Liu},
  journal={Journal of Cellular Biochemistry},
  year={2002},
  volume={86}
}
Fanconi anemia (FA), a genetic disorder predisposing to aplastic anemia and cancer, is characterized by hypersensitivity to DNA‐damaging agents and oxidative stress. Five of the cloned FA proteins (FANCA, FANCC, FANCE, FANCF, FANCG) appear to be involved in a common functional pathway that is required for the monoubiquitination of a sixth gene product, FANCD2. Here, we report that FANCA associates with the IκB kinase (IKK) signalsome via interaction with IKK2. Components of the FANCA complex… 
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The FANCA Gene and Its Products
TLDR
After completing this chapter the reader will gain an appreciation for the complexity of dissecting FANCA protein functions and for the importance of additional genetic, biochemical, and molecular analyses to interro­ gate FAN CA's role in maintaining genomic stability and regulating normal hematopoiesis.
Monoketone analogs of curcumin, a new class of Fanconi anemia pathway inhibitors
TLDR
Results suggest that monoketone analogs of curcumin are potent inhibitors of the FA pathway and constitute a promising new class of targeted anticancer compounds.
Genetic basis of Fanconi anemia
  • G. Bagby
  • Biology, Medicine
    Current opinion in hematology
  • 2003
Fanconi anemia is a rare autosomal recessive disease characterized by bone marrow failure, developmental anomalies, a high incidence of myelodysplasia and acute nonlymphocytic leukemia, and cellular…
Fanconi Anemia Proteins and Their Interacting Partners: A Molecular Puzzle
TLDR
The goal of this paper is to revisit old ideas and to discuss protein-protein interactions related to other FA-related molecular functions to try to give the reader a wider perspective of the FA molecular puzzle.
Defective mitochondrial peroxiredoxin-3 results in sensitivity to oxidative stress in Fanconi anemia
TLDR
A role for the FA proteins in mitochondria witsh sensitivity to oxidative stress resulting from diminished peroxidase activity is demonstrated, which may lead to apoptosis and the accumulation of oxidative DNA damage in bone marrow precursors.
oversecretion in Fanconi anemia α Aberrant activation of stress-response pathways leads to TNF
TLDR
It is demonstrated here that FANC pathway loss-of-function results in the aberrant activation of two major stress-signaling pathways: NF-κB and MAPKs, which normalizes TNF-α oversecretion in FA and provides a strong rationale for new clinical trials on FA patients.
AMP-activated protein kinase is involved in the activation of the Fanconi anemia/BRCA pathway in response to DNA interstrand crosslinks
TLDR
The data suggest AMPK is involved in the activation of the FA/BRCA pathway and shows that AMPKα interacted with FANCA, another component of theFA nuclear core complex.
Yeast two-hybrid screens imply involvement of Fanconi anemia proteins in transcription regulation, cell signaling, oxidative metabolism, and cellular transport.
Elevated levels of IL-1beta in Fanconi anaemia group A patients due to a constitutively active phosphoinositide 3-kinase-Akt pathway are capable of promoting tumour cell proliferation.
TLDR
It is demonstrated that the constitutive activation of the PI3K-Akt pathway in FA cells upregulates the expression of IL-1beta through an NF-kappaB-independent mechanism and that this overproduction activates the proliferation of tumour cells.
3R coordination by Fanconi anemia proteins.
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References

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TLDR
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TLDR
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