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anti-Human RIPK1 Antibodies:
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Human Polyclonal RIPK1 Primary Antibody for 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
Show all 4 Pubmed References
Human Polyclonal RIPK1 Primary Antibody for 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
Show all 2 Pubmed References
Human Polyclonal RIPK1 Primary Antibody for 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 for 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
Human Polyclonal RIPK1 Primary Antibody for 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
RIPK1-DD has a role in mediating RIPK1 dimerization and activation of its kinase activity during necroptosis and RIPK1-dependent apoptosis
We further identified this underlying mechanism also involved a PPARgamma (show PPARG Antibodies)-induced ANXA1 (show ANXA1 Antibodies)-dependent autoubiquitination of cIAP1 (show BIRC2 Antibodies), the direct E3 ligase of RIP1 (show UQCRFS1 Antibodies), shifting cIAP1 (show BIRC2 Antibodies) toward proteosomal degradation..our study provides first insight for the suitability of using drug-induced expression of ANXA1 (show ANXA1 Antibodies) as a new player in RIP1 (show UQCRFS1 Antibodies)-induced death machinery in triple-negative breast cancer
data suggest that artesunate could induce RIP1 (show UQCRFS1 Antibodies)-dependent cell death in human renal carcinoma (show TSC2 Antibodies).
RIP1 (show UQCRFS1 Antibodies) has a role in CD40 (show CD40 Antibodies)-mediated activation of caspase-8 (show CASP8 Antibodies), 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 (show FAM126A Antibodies)) patients after hepatectomy.
we found that ORF3 (show ASZ1 Antibodies) protein downregulates TLR3 (show TLR3 Antibodies)-mediated NF-kappaB (show NFKB1 Antibodies) signaling via TRADD (show TRADD Antibodies) and RIP1 (show UQCRFS1 Antibodies). 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 (show PARP1 Antibodies).
Study identify and quantify over 8,000 phosphorylated peptides, among which are numerous known sites in the TNF (show TNF Antibodies)-RSC, NFkappaB (show NFKB1 Antibodies), and MAP kinase (show MAPK1 Antibodies) signaling systems. Functional analysis of S320 phosphorylation in RIPK1 demonstrates a role for this event in suppressing its kinase activity, association with CASPASE-8 (show CASP8 Antibodies) and FADD (show FADD Antibodies) proteins, and subsequent necrotic cell death during inflammatory TNFalpha (show TNF Antibodies) stimulation.
We show that inflammation and autoimmunity are prevented upon expression of kinase inactive RIPK1 or deletion of RIPK3 (show RIPK3 Antibodies) or MLKL. We provide evidence that the inflammation is not driven by microbial ligands, but depends on the release of danger-associated molecular patterns and MyD88 (show MYD88 Antibodies)-dependent signaling.
RIPK1 kinase activity mediates TWEAK (show TNFSF12 Antibodies)-induced apoptosis.
The authors report here that male reproductive organs of both Ripk3 (show RIPK3 Antibodies)- 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 (show RIPK3 Antibodies) and MLKL. Moreover, it inhibits RIPK1 and RIPK3 (show RIPK3 Antibodies) kinase activity. In vivo Sorafenib protects against TNF (show TNF Antibodies)-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 (show TNF Antibodies) and downstream kinases such as RIPK1.
TNFalpha (show TNF Antibodies)-induced phosphorylation of RIPK1 in the intermediate domain by TAK1 (show NR2C2 Antibodies) 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.
Interaction of xFADD and xRIP1 induced synergistic activation of JNK (show MAPK8 Antibodies) and NF-kappaB (show NFKB1 Antibodies).
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