Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Aberrant activation of stress-response pathways leads to TNF-α oversecretion in Fanconi anemia

1 Dec 2007

Abstract excerpt

Fanconi anemia (FA), an inherited syndrome that associates bone marrow failure, cancer predisposition, and genetic instability, is characterized by an overproduction of the myelosuppressive cytokine TNF-alpha through unknown mechanisms. We demonstrate here that FANC pathway loss-of-function results in the aberrant activation of 2 major stress-signaling pathways: NF-kappaB and MAPKs. These responses are...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acute Myeloid Leukemia Research
Share to Cell death mechanisms and regulation
Share to DNA Repair Mechanisms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 18055871
DOI: 10.1182/blood-2007-07-099218

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Aberrant activation of stress-response pathways leads to TNF-α oversecretion in Fanconi anemiaPMID 18055871Read ↗

IL‐6, IL‐8, MMP‐2, MMP‐9 are overexpressed in Fanconi anemia cells through a NF‐κB/TNF‐α dependent mechanismSemantic proximity Read ↗

Inflammatory Reactive Oxygen Species-Mediated Hemopoietic Suppression in Fancc-Deficient MiceSemantic proximity Read ↗

A failure of TNFAIP3 negative regulation maintains sustained NF-κB activation in Sjögren’s syndromeSemantic proximity Read ↗

Inflammatory ROS promote and cooperate with the Fanconi anemia mutation for hematopoietic senescence.Semantic proximity Read ↗

Tumor necrosis factor-alpha and CD95 ligation suppress erythropoiesis in Fanconi anemia C gene knockout mice.Semantic proximity Read ↗

Direct inhibition of TNF-α promoter activity by Fanconi anemia protein FANCD2.Semantic proximity Read ↗

RGD-containing fibrillin-1 fragments upregulate matrix metalloproteinase expression in cell culture: A potential factor in the pathogenesis of the Marfan syndromeSemantic proximity Read ↗

p38 MAPK inhibition suppresses the TLR-hypersensitive phenotype in FANCC- and FANCA-deficient mononuclear phagocytes.Semantic proximity Read ↗

Gene-Dose Effect of MEFV Gain-of-Function Mutations Determines ex vivo Neutrophil Activation in Familial Mediterranean Fever.Semantic proximity Read ↗

Mutations in calcium-binding epidermal growth factor modules render fibrillin-1 susceptible to proteolysis. A potential disease-causing mechanism in Marfan syndrome.Semantic proximity Read ↗

Reduced tumor necrosis factor signaling in primary human fibroblasts containing a tumor necrosis factor receptor superfamily 1A mutant.Semantic proximity Read ↗

Abnormal tumor necrosis factor receptor I cell surface expression and NF-kappaB activation in tumor necrosis factor receptor-associated periodic syndrome.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.