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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
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Human Monoclonal RIPK1 Primary Antibody for IP, WB - ABIN532716
Festjens, Vanden Berghe, Cornelis, Vandenabeele: RIP1, a kinase on the crossroads of a cell's decision to live or die. in Cell death and differentiation 2007
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Human Polyclonal RIPK1 Primary Antibody for WB - ABIN3042930
Chen, Zhao, Wu, Zou, Luo, Li, Xie, Liang: The role of RIP1 and RIP3 in the development of aplastic anemia induced by cyclophosphamide and busulphan in mice. in International journal of clinical and experimental pathology 2015
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Human Polyclonal RIPK1 Primary Antibody for WB - ABIN3042480
Wang, Ma, Hu, Xie, Wu, Zeng, Song: Bifidobacterial recombinant thymidine kinase-ganciclovir gene therapy system induces FasL and TNFR2 mediated antitumor apoptosis in solid tumors. in BMC cancer 2017
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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
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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
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 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
The caspase 8 mediated RIPK1 cleavage product has a pro-apoptotic function, and further cleavage of this pro-apoptotic cleavage product by human rhinovirus 3C protease may provide a mechanism by which human rhinovirus limits apoptosis.
The major function of RIP1 kinase activity in TNF-induced necroptosis is to autophosphorylate serine 161. This specific phosphorylation then enables RIP1 to recruit RIP3 and form a functional necrosome, a central controller of necroptosis.
In lesional psoriatic epidermis, RIPK1-expression was decreased compared with that in normal epidermis. RIPK1-knockdown enhanced TRAIL-mediated expression of psoriasis-relating cytokines in normal human epidermal keratinocytes.
RIPK1 plays a critical role in the human immune system.
Elevated A20 promotes TNF-induced and RIPK1-dependent intestinal epithelial cell death
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-induced ANXA1-dependent autoubiquitination of cIAP1, the direct E3 ligase of RIP1, shifting cIAP1 toward proteosomal degradation..our study provides first insight for the suitability of using drug-induced expression of ANXA1 as a new player in RIP1-induced death machinery in triple-negative breast cancer
data suggest that artesunate could induce RIP1-dependent cell death in human renal carcinoma.
RIP1 has a role in CD40-mediated activation of caspase-8, 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) patients after hepatectomy.
we found that ORF3 protein downregulates TLR3-mediated NF-kappaB signaling via TRADD and RIP1. 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.
Study identify and quantify over 8,000 phosphorylated peptides, among which are numerous known sites in the TNF-RSC, NFkappaB, and MAP kinase signaling systems. Functional analysis of S320 phosphorylation in RIPK1 demonstrates a role for this event in suppressing its kinase activity, association with CASPASE-8 and FADD proteins, and subsequent necrotic cell death during inflammatory TNFalpha stimulation.
New potent RIPK1 inhibitors are reported (GSK2606414 and GSK2656157).
In conclusion, for the first time, we report that TRADD, TRAF2, RIP1 and TAK1 play a role in the regulating TNF-alpha signalling in human myometrium. These findings are of significance given the central role of TNF-alpha in the processes of human labour and delivery.
the in vivo effects were diametrically reversed with RIP3 deletion or RIP1 blockade, resulting in marked tumor protection. The dichotomy between the in vivo and in vitro results suggests that the microenvironmental milieu resulting from RIP1/RIP3 signaling is likely responsible for its protumorigenic effects
Shikonin induces glioma cell necroptosis in vitro by reactive oxygen species overproduction and promoting RIP1/RIP3 necrosome formation.
the cytoplasmic retinoic acid receptor gamma (RARgamma) controls receptor-interacting protein kinase 1 (RIP1)-initiated cell death when cellular inhibitor of apoptosis (cIAP) activity is blocked.
Ischemia induces an up-regulation of RIP1K and an enhancement of RIP1K-RIP3K complex formation in neurons and astrocytes. Inhibition of RIP1K increases ischemia-induced reduction in MAP2 or GFAP and decreases ischemia-induced neuronal or astrocytic cell necrosis in the ischemic cortex, and directly protects OGD-induced neuronal or astrocytic cell death. Nec-1 blocks RIP1K-RIP3K complex formation.
Aldehyde dehydrogenase 2 deficiency negates chronic low-to-moderate alcohol consumption-induced cardioprotecion possibly via ROS-dependent apoptosis and RIP1/RIP3/MLKL-mediated necroptosis.
two different modes of necroptosis induction by TNFalpha exist which are differentially regulated by iuRIPK1 formation. Overall, this work reveals a distinct mechanism of RIPK1 activation that mediates the signaling mechanism of RDA as well as a type of necroptosis.
We show that inflammation and autoimmunity are prevented upon expression of kinase inactive RIPK1 or deletion of RIPK3 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-dependent signaling.
RIPK1 kinase activity mediates TWEAK-induced apoptosis.
The authors report here that male reproductive organs of both Ripk3- 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 and MLKL. Moreover, it inhibits RIPK1 and RIPK3 kinase activity. In vivo Sorafenib protects against TNF-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 and downstream kinases such as RIPK1.
TNFalpha-induced phosphorylation of RIPK1 in the intermediate domain by TAK1 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 1 (RIPK1) is required for Yersinia-induced apoptosis.
p38MAPK/MK2 phosphorylation of RIPK1 is a crucial checkpoint for cell fate in inflammation and infection that determines the outcome of bacteria-host cell interaction.
MK2-mediated RIPK1 phosphorylation is an important molecular mechanism limiting the sensitivity of the cells to the cytotoxic effects of TNF.
An alternative function for RIPK1/RIPK3 in vascular permeability.
these results revealed a novel, kinase-independent function of RIP1, which is essential for not only promoting TCR-induced proliferative responses but also in blocking apoptosis in mature T cells.
Interaction of xFADD and xRIP1 induced synergistic activation of JNK and NF-kappaB.
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