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FLASH GENE

Symbol

TNFRSF1B

contributors: mct/npt - updated : 15-04-2014

HGNC name	tumor necrosis factor receptor superfamily, member 1B
HGNC id	11917

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	four extracytoplasmic cysteine-rich pseudorepeats typical for the TNFR superfamily
	a preligand assembly domain (PLAD) in CRD1 mediating ligand-independent receptor assembly and signaling
	a small cytoplasmic domain with the serine/threonine kinase but lacking a DEATH domain

mono polymer

homomer , trimer

HOMOLOGY

Homologene

FAMILY

tumor necrosis factor receptor superfamily

CATEGORY

signaling cytokine , receptor

SUBCELLULAR LOCALIZATION	extracellular
	plasma membrane
	intracellular,nucleus
	intracellular,nuclear envelope
text	type I transmembrane protein

basic FUNCTION	may be playing a role in protecting neurons from apoptosis by stimulating antioxidative pathways
	leading to selective ASK1 ubiquitination and degradation in proteasomes
	leading to TRAF2 ubiquitination and subsequent proteasomal degradation
	endogenous TNFRSF1B/TNFRSF1A signaling pathway in polymicrobial sepsis reduces neutrophil recruitment contributing to mortality
	critical role for endothelial TNFR2 in ischemia-mediated adaptive angiogenesis
	through TNFRSF1B, microglia may contribute to the counter-regulatory response activated in neuropathological conditions
	is involved in tissue regeneration and neuroprotection
	TNFRSF1A, TNFRSF1B were required for IRF1-IFNB signaling and, in human endothelial cells
	TNFRSF1A, TNFRSF1B activities are required for the TNF-induced proinflammatory response
	potential mechanism for the neuroprotective role of TNFRSF1B in oligodendrocyte progenitor cells (OPCs)
	can protect OPCs from oxidative stress by expression of anti-apoptotic proteins and further underscore the potential of TNFRSF1B in neuroregenerative processes

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

a component

TNFRSF1B/SMURF2 complex

INTERACTION

DNA

RNA

small molecule

protein	interacting with SMURF2 and TRAF2 (SMURF2-induced TNFRSF1B ubiquitination and subcellular relocalization of TNFRSF1B and TRAF2 enables the specific activation of the JNK pathway)
	ASB3 is a negative regulator of TNFRSF1B-mediated cellular responses to TNF by direct targeting of TNFRSF1B for ubiquitination and proteasome-mediated degradation
	may contribute to the tumor-promoting roles of STAT3
	PADI2 regulates the expression of the TNFRSF1B, ADAMTS9, and RAB6B transcripts in mast cells
	TNFRSF1B-dependent homeostasis of regulatory T cells as a player in TNF-induced experimental metastasis
	TRAF2 is critical for either TNFRSF1A- or TNFRSF1B-mediated activation of NFKB and mitogen-activated protein kinase (MAPK) signaling, as well as for target gene expression
	XPNPEP3-mediated TNFRSF1B signal transduction mechanism that induces activation of MAPK8 and MAPK9

cell & other

REGULATION

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral   deletion     in neuroblastoma

Susceptibility

to familial combined hyperlipidemia to systemic lupus erythematosis and to narcolepsy to coronary artery disease and to osteoporosis to Mycobacterium tuberculosis infection

Variant & Polymorphism other	A593 - T598 - C620 haplotype decreased bone mineral density
	functional haplotype in the 3 prime untranslated region of TNFRSF1B is associated with tuberculosis

Candidate gene
Marker
Therapy target
	System Type Disorder Pubmed neurology neurodegenerative   activation of TNFSF1B signaling by TNC-scTNFSF1B appears a promising strategy to ameliorate neurodegenerative processes.

ANIMAL & CELL MODELS