Anti-RIP antibody [EPR19697],Abcam,AB202985

Patented technology Our RabMAb ® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb ® patents . What are the advantages of a recombinant monoclonal antibody? This product is a recombinant monoclonal antibody, which offers several advantages including: - High batch-to-batch consistency and reproducibility - Improved sensitivity and specificity - Long-term security of supply - Animal-free batch production For more information, read more on recombinant antibodies .

Host

Rabbit

Reactivity

Mouse

Application

Flow Cyt (Intra), WB, IP, ICC/IF

Platform ID

BAB082537128

Abcam

Headquarters

Discovery Drive Cambridge Biomedical Campus Cambridge CB2 0AX UK

Contact

Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215

Product Specifications
Scientific Background

Specifications

NameAnti-RIP antibody [EPR19697]
Cat. No.AB202985
HostRabbit
IsotypeIgG
ReactivityMouse
ApplicationFlow Cyt (Intra), WB, IP, ICC/IF
ClonalityMonoclonal
Clone NumberEPR19697
Concentration0.568 mg/mL Batch dependent concentration
ImmunogenThe exact immunogen used to generate this antibody is proprietary information.
PurityAffinity purification Protein A
Appearance/FormLiquid
ShippingBlue Ice
FormulationpH: 7.2 - 7.4 Preservative: 0.01% Sodium azide Constituents: PBS, 40% Glycerol (glycerin, glycerine), 0.05% BSA
Storage-20°C
Regulatory StatusResearch Use Only

Scientific Background

Target data Serine-threonine kinase which is a key regulator of TNF-mediated apoptosis, necroptosis and inflammatory pathways (PubMed : 24557836, PubMed : 24813849, PubMed : 24813850, PubMed : 27819681, PubMed : 28842570, PubMed : 31511692, PubMed : 31827280, PubMed : 31827281, PubMed : 33397971). Exhibits kinase activity-dependent functions that regulate cell death and kinase-independent scaffold functions regulating inflammatory signaling and cell survival (PubMed : 24557836, PubMed : 24813849, PubMed : 24813850, PubMed : 28842570, PubMed : 31519886, PubMed : 31519887). Has kinase-independent scaffold functions : upon binding of TNF to TNFR1, RIPK1 is recruited to the TNF-R1 signaling complex (TNF-RSC also known as complex I) where it acts as a scaffold protein promoting cell survival, in part, by activating the canonical NF-kappa-B pathway (PubMed : 31519886, PubMed : 31519887). Kinase activity is essential to regulate necroptosis and apoptosis, two parallel forms of cell death : upon activation of its protein kinase activity, regulates assembly of two death-inducing complexes, namely complex IIa (RIPK1-FADD-CASP8), which drives apoptosis, and the complex IIb (RIPK1-RIPK3-MLKL), which drives necroptosis (PubMed : 27819681, PubMed : 27819682, PubMed : 28842570, PubMed : 29440439, PubMed : 30988283, PubMed : 31519886, PubMed : 31519887). RIPK1 is required to limit CASP8-dependent TNFR1-induced apoptosis (PubMed : 24557836, PubMed : 24813849, PubMed : 24813850). In normal conditions, RIPK1 acts as an inhibitor of RIPK3-dependent necroptosis, a process mediated by RIPK3 component of complex IIb, which catalyzes phosphorylation of MLKL upon induction by ZBP1 (PubMed : 24557836, PubMed : 27819681, PubMed : 27819682, PubMed : 31358656). Inhibits RIPK3-mediated necroptosis via FADD-mediated recruitment of CASP8, which cleaves RIPK1 and limits TNF-induced necroptosis (PubMed : 31358656). Required to inhibit apoptosis and necroptosis during embryonic development : acts by preventing the interaction of TRADD with FADD thereby limiting aberrant activation of CASP8 (PubMed : 30185824, PubMed : 30867408). In addition to apoptosis and necroptosis, also involved in inflammatory response by promoting transcriptional production of pro-inflammatory cytokines, such as interleukin-6 (IL6) (PubMed : 31827280, PubMed : 31827281). Phosphorylates RIPK3 : RIPK1 and RIPK3 undergo reciprocal auto- and trans-phosphorylation (By similarity). Phosphorylates DAB2IP at 'Ser-728' in a TNF-alpha-dependent manner, and thereby activates the MAP3K5-JNK apoptotic cascade (By similarity). Required for ZBP1-induced NF-kappa-B activation in response to DNA damage (PubMed : 12654725, PubMed : 19590578). See full target information Ripk1

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