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Data suggest that Fas (zeige FAS Proteine) and TNFR1 are involved in glaucoma mechanisms in cornea; pro-apoptotic effect of anti-glaucoma medication clonidine on corneal epithelial cells triggers Fas (zeige FAS Proteine)/TNFR1-mediated, mitochondria-dependent signaling pathway. (Fas (zeige FAS Proteine) = Fas (zeige FAS Proteine) cell surface death receptor ; TNFR1 = TNF (zeige TNF Proteine) receptor superfamily member 1A)
These results indicate that TNFRI-Fc and hHO-1 overexpression may apparently induce free iron in the liver and exert oxidative stress by enhancing reactive oxygen species production and block normal postneonatal liver metabolism.
Data suggest that elevated serum levels of soluble TNF (zeige TNF Proteine) receptors, especially sTNFR1, are associated with loss of kidney function in Hispanic patients with diabetes type 2 in Colombia.
Case Report: heterozygous missense variants in TNFRSF1A identified in family members with familial Mediterranean fever (zeige MEFV Proteine).
Case Report: autoinflammatory syndrome with relapsing aseptic neutrophilic meningitis and chronic myelitis associated with MEFV (zeige MEFV Proteine)/TNFRSF1A mutations.
In this article we will review the role of ubiquitination and proteolysis in these diverse events focusing on our own contributions to the lysosomal apoptotic pathway linked to the subcellular compartmentalization of TNF-R1
Coadministration of either ATROSAB or EHD2 (zeige EHD2 Proteine)-scTNFR2 into the magnocellular nucleus basalis significantly protected cholinergic neurons and their cortical projections against cell death, and reverted the neurodegeneration-associated memory impairment in a passive avoidance paradigm. Simultaneous blocking of TNFR1 and TNFR2 (zeige TNFRSF1B Proteine) signaling, however, abrogated the therapeutic effect
after 14 days of glucocorticoid therapy, clinical findings (serum bilirubin, skin GVHD) and plasma biomarkers (TIM3, ST2, sTNFR1) can predict failure of GVHD treatment and nonrelapse mortality.
Data show that interleukin-2 receptor alpha (zeige IL2RA Proteine), tumor necrosis factor receptor 1, serum STimulation-2 (IL1RL1 (zeige IL1RL1 Proteine) gene product), and regenerating islet-derived 3-alpha (zeige REG3A Proteine) were significantly associated with non-relapse mortality.
Report of a severe case of TRAPS associated with a novel mutation, Thr90Pro, in the TNFRSF1A gene in an infant and several family members.
These findings indicate that TNFR1 is structurally positioned to modulate postsynaptic signaling in the PVN, suggesting a mechanism whereby TNFR1 activation contributes to cardiovascular and other autonomic functions.
Increased TNFR1 expression and signaling in injured peripheral nerves of mice with reduced BACE1 (zeige BACE Proteine) activity
Results show that interleukin 6 (IL6 (zeige IL6 Proteine)) promotes oval cell proliferation and liver regeneration, while tumor necrosis factor alpha (TNFalpha (zeige TNF Proteine)) and TNF (zeige TNF Proteine) receptor-1(TNFR1) do not affect this process.
Data suggest that dietary treatment with green tea extract reduces hepatic inflammation in non-alcoholic fatty liver disease by decreasing proinflammatory signaling in liver through Tnfr1 (tumor necrosis factor (zeige TNF Proteine) receptor superfamily, member 1a) and Tlr4 (toll-like receptor 4 (zeige TLR4 Proteine)) that otherwise increases NFkappaB activation and liver injury.
Genetic deletion of TNFR1 completely blocks TNF-alpha (zeige TNF Proteine)-induced inflammation and reduces allergen-induced inflammation. Preserved electro-olfactogram responses suggest a TNFR1-dependent mechanism of TNF-alpha (zeige TNF Proteine)-induced olfactory neuron dysfunction.
This work uncovers a dichotomy of function for TNFR2 (zeige TNFRSF1B Proteine) in myeloid cells, with microglial TNFR2 (zeige TNFRSF1B Proteine) providing protective signals to contain disease and monocyte/macrophagic TNFR2 (zeige TNFRSF1B Proteine) driving immune activation and experimental autoimmune encephalomyelitis initiation.
The deficiency of TNFRp55 promoted the development of endometriosis.
TNFalpha (zeige TNF Proteine) enhanced murine NK cell IFNgamma production via TNFR2 (zeige TNFRSF1B Proteine) in vitro
TNFR2 (zeige TNFRSF1B Proteine) sensitizes macrophages for endogenous TNF (zeige TNF Proteine)-induced TNFR1-mediated necroptosis
this study shows that epithelial TNFR1 signaling promotes mucosal repair in inflammatory bowel disease
Retinal ischemia results in increased expression of TNF-alpha (zeige TNF Proteine) and its receptors (TNF-R1 and TNF-R2 (zeige TNFRSF1B Proteine)).
Targeted gene knockdown of TNFRSF1B (zeige TNFRSF1B Proteine) in zebrafish embryos results in the induction of a caspase-8 (zeige CASP8 Proteine), caspase-2 (zeige CASP2 Proteine) and P53 (zeige TP53 Proteine)-dependent apoptotic program in endothelial cells that bypasses caspase-3 (zeige CASP3 Proteine).
These results suggest that TNF-alpha (zeige TNF Proteine) sources include immune cells, as well as large and small luteal cells, and that TNF-RI and TNF-RII (zeige TNFRSF1B Proteine) are present in the luteal cells of the bovine corpus luteum.
The expression and cellular localization of tumor necrosis factor-alpha (TNF (zeige TNF Proteine)) and its receptors (TNFRI and TNFRII (zeige TNFRSF1B Proteine)) mRNAs and proteins, were determined.
The upregulation of TNFRI mRNA expression by IFNG (zeige IFNG Proteine) suggests that TNF (zeige TNF Proteine) and IFNG (zeige IFNG Proteine) synergistically affect the death of luteal endothelial cells resulting in acute luteolysis
TNF (zeige TNF Proteine) binding induces release of AIP1 (DAB2IP (zeige DAB2IP Proteine)) from TNFR1, resulting in cytoplasmic translocation and concomitant formation of an intracellular signaling complex comprised of TRADD (zeige TRADD Proteine), RIP1 (zeige RALBP1 Proteine), TRAF2 (zeige TRAF2 Proteine), and AIPl.
The protein encoded by this gene is a member of the TNF-receptor superfamily. This protein is one of the major receptors for the tumor necrosis factor-alpha. This receptor can activate NF-kappaB, mediate apoptosis, and function as a regulator of inflammation. Antiapoptotic protein BCL2-associated athanogene 4 (BAG4/SODD) and adaptor proteins TRADD and TRAF2 have been shown to interact with this receptor, and thus play regulatory roles in the signal transduction mediated by the receptor. Germline mutations of the extracellular domains of this receptor were found to be associated with the autosomal dominant periodic fever syndrome. The impaired receptor clearance is thought to be a mechanism of the disease.
, tumor necrosis factor binding protein 1
, tumor necrosis factor receptor 1A isoform beta
, tumor necrosis factor receptor superfamily member 1A
, tumor necrosis factor receptor type 1
, tumor necrosis factor-alpha receptor
, TNF receptor alpha chain
, tumor necrosis factor receptor 1
, tumor necrosis factor receptor type I
, p55 TNF receptor
, tumor necrosis factor receptor p60
, TNF Receptor 1 (TR1)
, tumor necrosis factor type I
, tumor necrosis factor receptor superfamily, member 1A
, tumor necrosis factor receptor superfamily member 1A-like