描述：
TWEAK is a type II transmembrane protein belonging to the TNF superfamily.
It contains a short cytoplasmic domain (aa 1 18), the transmembrane domain
(aa 19 42) and an extracellular domain (aa 43 249). The extracellular domains
of human and murine TWEAK share 89% aa sequence identity. A soluble form
of TWEAK is generated from the membraneassociated molecules by proteolytic
cleavage after Arg 93 suggesting that TWEAK may have longrange effects.
TWEAK is expressed widely in many tissues and cells. At least two receptors that
bind TWEAK have been identified. Death Receptor 3 (DR3), also known as TNFRSF12,
Apo3, LARD, WSL1 or TRAMP, is a TNF receptor superfamily member that is
expressed predominantly in tissues with high lymphocyte content. It has been
suggested that induction of cell death by TWEAKDR3 interaction involves the
activation of NFκB. In cells that lack DR3, alternate pathways of TWEAKinduced cell
death mediated by receptors distinct from DR3 have been suggested. TWEAK
receptor (TWEAKR, alternatively known as FN14), is a novel TNF receptor superfamily
member that also binds TWEAK. It is a mitogeninducible gene that is expressed in
fibroblasts, hepetocellular carcinomas and endothelial cells. TWEAKTWEAKR
interaction has been shown to play a role in endothelial cell growth and migration.
This effect of TWEAK is not mediated by an upregulation of VEGF.
原厂资料：
TWEAK is a type II transmembrane protein belonging to the TNF superfamily.
It contains a short cytoplasmic domain (aa 1 18), the transmembrane domain
(aa 19 42) and an extracellular domain (aa 43 249). The extracellular domains
of human and murine TWEAK share 89% aa sequence identity. A soluble form
of TWEAK is generated from the membraneassociated molecules by proteolytic
cleavage after Arg 93 suggesting that TWEAK may have longrange effects.
TWEAK is expressed widely in many tissues and cells. At least two receptors that
bind TWEAK have been identified. Death Receptor 3 (DR3), also known as TNFRSF12,
Apo3, LARD, WSL1 or TRAMP, is a TNF receptor superfamily member that is
expressed predominantly in tissues with high lymphocyte content. It has been
suggested that induction of cell death by TWEAKDR3 interaction involves the
activation of NFκB. In cells that lack DR3, alternate pathways of TWEAKinduced cell
death mediated by receptors distinct from DR3 have been suggested. TWEAK
receptor (TWEAKR, alternatively known as FN14), is a novel TNF receptor superfamily
member that also binds TWEAK. It is a mitogeninducible gene that is expressed in
fibroblasts, hepetocellular carcinomas and endothelial cells. TWEAKTWEAKR
interaction has been shown to play a role in endothelial cell growth and migration.
This effect of TWEAK is not mediated by an upregulation of VEGF.
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