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Human Polyclonal RIPK1 Primary Antibody für ELISA, ICC - ABIN4350584
Nilsson, Loganathan, Sekiguchi, Matsuba, Hui, Tsubuki, Tanaka, Iwata, Saito, Saido: Aβ secretion and plaque formation depend on autophagy. in Cell reports 2013
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Human Polyclonal RIPK1 Primary Antibody für IF (p), IHC (p) - ABIN715016
Luo, Roy, Xiao, Sun, Liang, Chen, Fu, Sun, Zhu, Ye, Liu: Lycorine induces programmed necrosis in the multiple myeloma cell line ARH-77. in Tumour biology 2014
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Human Polyclonal RIPK1 Primary Antibody für ICC, IF - ABIN4350585
Hirsch, von der Wall, Hummel, Dürkop: RIP1 expression is necessary for CD30-mediated cell death induction in anaplastic large-cell lymphoma cells. in Laboratory investigation; a journal of technical methods and pathology 2013
Human Polyclonal RIPK1 Primary Antibody für IF (p) - ABIN715023
Seifert, Werba, Tiwari, Giao Ly, Alothman, Alqunaibit, Avanzi, Barilla, Daley, Greco, Torres-Hernandez, Pergamo, Ochi, Zambirinis, Pansari, Rendon, Tippens, Hundeyin, Mani, Hajdu, Engle, Miller: The necrosome promotes pancreatic oncogenesis via CXCL1 and Mincle-induced immune suppression. in Nature 2016
Human Polyclonal RIPK1 Primary Antibody für IHC, IHC (p) - ABIN4350581
Ratovitski: Phospho-ΔNp63α-responsive microRNAs contribute to the regulation of necroptosis in squamous cell carcinoma upon cisplatin exposure. in FEBS letters 2015
RIP1 (zeige UQCRFS1 Antikörper) has a role in CD40 (zeige CD40 Antikörper)-mediated activation of caspase-8 (zeige CASP8 Antikörper), which in turn leads to induction of apoptosis
High RIPK1 expression is associated with Alzheimer's disease.
These data represent the first report of decreased RIPK1 expression in neutrophils of Systemic Lupus Erythematosus patients and imply that RIPK1 may be involved in neutrophil death and neutrophil extracellular traps formation.
Data indicate that receptor (TNFRSF)-interacting serine-threonine kinase 1 (RIPK1) polymorphism is a prognostic biomarker for tumor development and survival of hepatocellular carcinoma (HCC (zeige FAM126A Antikörper)) patients after hepatectomy.
we found that ORF3 (zeige ASZ1 Antikörper) protein downregulates TLR3 (zeige TLR3 Antikörper)-mediated NF-kappaB (zeige NFKB1 Antikörper) signaling via TRADD (zeige TRADD Antikörper) and RIP1 (zeige UQCRFS1 Antikörper). Our findings provide a new perspective on the cellular response in HEV infection and expand our understanding of the molecular mechanisms of Hepatitis E virus (HEV) pathogenesis in innate immunity.
Existence of a kinase-independent role of nuclear RIPK1 in the regulation of PARP1 (zeige PARP1 Antikörper).
Study identify and quantify over 8,000 phosphorylated peptides, among which are numerous known sites in the TNF (zeige TNF Antikörper)-RSC, NFkappaB (zeige NFKB1 Antikörper), and MAP kinase (zeige MAPK1 Antikörper) signaling systems. Functional analysis of S320 phosphorylation in RIPK1 demonstrates a role for this event in suppressing its kinase activity, association with CASPASE-8 (zeige CASP8 Antikörper) and FADD (zeige FADD Antikörper) proteins, and subsequent necrotic cell death during inflammatory TNFalpha (zeige TNF Antikörper) stimulation.
New potent RIPK1 inhibitors are reported (GSK2606414 and GSK2656157).
In conclusion, for the first time, we report that TRADD (zeige TRADD Antikörper), TRAF2 (zeige TRAF2 Antikörper), RIP1 (zeige UQCRFS1 Antikörper) and TAK1 (zeige MAP3K7 Antikörper) play a role in the regulating TNF-alpha (zeige TNF Antikörper) signalling in human myometrium. These findings are of significance given the central role of TNF-alpha (zeige TNF Antikörper) in the processes of human labour and delivery.
the in vivo effects were diametrically reversed with RIP3 (zeige RIPK3 Antikörper) deletion or RIP1 (zeige UQCRFS1 Antikörper) blockade, resulting in marked tumor protection. The dichotomy between the in vivo and in vitro results suggests that the microenvironmental milieu resulting from RIP1 (zeige UQCRFS1 Antikörper)/RIP3 (zeige RIPK3 Antikörper) signaling is likely responsible for its protumorigenic effects
The authors report here that male reproductive organs of both Ripk3 (zeige RIPK3 Antikörper)- and Mlkl-knockout mice retain 'youthful' morphology and function into advanced age, while those of age-matched wild-type mice deteriorate. Feeding of wild-type mice with an RIPK1 inhibitor prior to the normal onset of age-related changes in their reproductive organs blocked the appearance of signs of aging.
Pull down experiments with biotinylated Sorafenib show that it binds independently RIPK1, RIPK3 (zeige RIPK3 Antikörper) and MLKL. Moreover, it inhibits RIPK1 and RIPK3 (zeige RIPK3 Antikörper) kinase activity. In vivo Sorafenib protects against TNF (zeige TNF Antikörper)-induced systemic inflammatory response syndrome (SIRS) and renal ischemia-reperfusion injury (IRI).
The study provides genetic evidence that different RIP1 kinase inactive mutations have distinct impacts on the embryogenesis of Fadd-deficient mice.
Excessive death of hepatocytes is a characteristic of liver injury. A new programmed cell death pathway has been described involving upstream death ligands such as TNF (zeige TNF Antikörper) and downstream kinases such as RIPK1.
TNFalpha (zeige TNF Antikörper)-induced phosphorylation of RIPK1 in the intermediate domain by TAK1 (zeige NR2C2 Antikörper) plays a key role in regulating the decision between three distinct mechanisms of cell death: necroptosis, RIPK1-independent and dependent apoptosis.
K45 mediated kinase activity of RIPK1 is not only important for necroptosis but it also has a key role in promoting cytokine signaling and host response to inflammatory stimuli.
Data show that the kinase activity of receptor-interacting protein kinase (zeige CDK7 Antikörper) 1 (RIPK1) is required for Yersinia-induced apoptosis.
p38MAPK (zeige MAPK14 Antikörper)/MK2 (zeige KCNA2 Antikörper) phosphorylation of RIPK1 is a crucial checkpoint for cell fate in inflammation and infection that determines the outcome of bacteria-host cell interaction.
MK2 (zeige KCNA2 Antikörper)-mediated RIPK1 phosphorylation is an important molecular mechanism limiting the sensitivity of the cells to the cytotoxic effects of TNF (zeige TNF Antikörper).
Interaction of xFADD and xRIP1 induced synergistic activation of JNK (zeige MAPK8 Antikörper) and NF-kappaB (zeige NFKB1 Antikörper).
Serine-threonine kinase which transduces inflammatory and cell-death signals (necroptosis) following death receptors ligation, activation of pathogen recognition receptors (PRRs), and DNA damage. Upon activation of TNFR1 by the TNF-alpha family cytokines, TRADD and TRAF2 are recruited to the receptor. Ubiquitination by TRAF2 via 'Lys-63'-link chains acts as a critical enhancer of communication with downstream signal transducers in the mitogen-activated protein kinase pathway and the NF-kappa-B pathway, which in turn mediate downstream events including the activation of genes encoding inflammatory molecules. Polyubiquitinated protein binds to IKBKG/NEMO, the regulatory subunit of the IKK complex, a critical event for NF-kappa-B activation. Interaction with other cellular RHIM-containing adapters initiates gene activation and cell death. RIPK1 and RIPK3 association, in particular, forms a necroptosis-inducing complex.
, cell death protein RIP
, receptor interacting protein
, receptor-interacting protein 1
, receptor-interacting serine/threonine-protein kinase 1
, serine/threonine-protein kinase RIP
, receptor (TNFRSF)-interacting serine-threonine kinase 1
, receptor interacting serine/threonine kinase 1 L homeolog
, receptor-interacting protein 1 beta