(Q35849941)

English

Abnormal disulfide-linked oligomerization results in ER retention and altered signaling by TNFR1 mutants in TNFR1-associated periodic fever syndrome (TRAPS)

scientific article published on 9 May 2006

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scholarly article

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

Abnormal disulfide-linked oligomerization results in ER retention and altered signaling by TNFR1 mutants in TNFR1-associated periodic fever syndrome (TRAPS) (English)

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

periodic fever syndrome

1 reference

based on heuristic

inferred from title

Gavin R Screaton

object named as

Gavin R Screaton

8

0 references

Daniel L. Kastner

7

object named as

Daniel L Kastner

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

author name string

Adrian A Lobito

1

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

Fiona C Kimberley

2

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

Jagan R Muppidi

3

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

Hirsh Komarow

4

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

Adrianna J Jackson

5

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

Keith M Hull

6

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

Richard M Siegel

9

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

language of work or name

0 references

publication date

9 May 2006

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

108

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

4

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

1320-1327

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

Mutation of the extracellular domain of tumour necrosis factor receptor 1 causes reduced NF-kappaB activation due to decreased surface expression

1 reference

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Tumor necrosis factor receptor I from patients with tumor necrosis factor receptor-associated periodic syndrome interacts with wild-type tumor necrosis factor receptor I and induces ligand-independent NF-kappaB activation.

1 reference

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Reduced tumor necrosis factor signaling in primary human fibroblasts containing a tumor necrosis factor receptor superfamily 1A mutant

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1895878

11 July 2018

ER stress and the unfolded protein response

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1895878

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Mutant forms of tumour necrosis factor receptor I that occur in TNF-receptor-associated periodic syndrome retain signalling functions but show abnormal behaviour.

1 reference

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Analysis of human tumour necrosis factor receptor 1 dominant-negative mutants reveals a major region controlling cell surface expression

1 reference

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Activation of endoplasmic reticulum-specific stress responses associated with the conformational disease Z alpha 1-antitrypsin deficiency.

1 reference

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Release of full-length 55-kDa TNF receptor 1 in exosome-like vesicles: a mechanism for generation of soluble cytokine receptors

1 reference

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Heterogeneity among patients with tumor necrosis factor receptor-associated periodic syndrome phenotypes

1 reference

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Tumor necrosis factor signaling.

1 reference

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11 July 2018

Quality control in the endoplasmic reticulum

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1895878

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The TNF receptor-associated periodic syndrome (TRAPS): emerging concepts of an autoinflammatory disorder

1 reference

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The p55 tumour necrosis factor receptor TNFR1 contains a trans-Golgi network localization signal in the C-terminal region of its cytoplasmic tail.

1 reference

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DeltaF508-CFTR causes constitutive NF-kappaB activation through an ER-overload response in cystic fibrosis lungs

1 reference

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Measurement of molecular interactions in living cells by fluorescence resonance energy transfer between variants of the green fluorescent protein

1 reference

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11 July 2018

The tumor-necrosis-factor receptor-associated periodic syndrome: new mutations in TNFRSF1A, ancestral origins, genotype-phenotype studies, and evidence for further genetic heterogeneity of periodic fevers

1 reference

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The multifaceted role of Fas signaling in immune cell homeostasis and autoimmunity

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Fas preassociation required for apoptosis signaling and dominant inhibition by pathogenic mutations

1 reference

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A domain in TNF receptors that mediates ligand-independent receptor assembly and signaling

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1895878

11 July 2018

Golgi membranes are absorbed into and reemerge from the ER during mitosis

1 reference

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11 July 2018

Autoimmune lymphoproliferative syndrome with defective Fas: genotype influences penetrance

1 reference

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Aggresomes: a cellular response to misfolded proteins

1 reference

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TNF-dependent recruitment of the protein kinase RIP to the TNF receptor-1 signaling complex

1 reference

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TRADD-TRAF2 and TRADD-FADD interactions define two distinct TNF receptor 1 signal transduction pathways

1 reference

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Crystal structure of the soluble human 55 kd TNF receptor-human TNF beta complex: implications for TNF receptor activation

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Expression of influenza virus hemagglutinin activates transcription factor NF-kappa B.

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The TNF receptor 1-associated protein TRADD signals cell death and NF-kappa B activation

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Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome

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Ligand-independent redistribution of Fas (CD95) into lipid rafts mediates clonotypic T cell death.

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Germline mutations in the extracellular domains of the 55 kDa TNF receptor, TNFR1, define a family of dominantly inherited autoinflammatory syndromes.

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Activation of transcription factor NF-kappaB by the adenovirus E3/19K protein requires its ER retention

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1 reference

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1 reference

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1 reference

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inferred from PubMed ID database lookup

Identifiers

10.1182/BLOOD-2005-11-006783

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

PMC publication ID

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

PubMed publication ID

1 reference

Europe PubMed Central

PMC publication ID

10 August 2017

ResearchGate publication ID

0 references

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