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RIP antibody

Cat. No. GTX10427

Host

Rabbit

Clonality

Polyclonal

Isotype

IgG

Application

WB

Reactivity

Human
Package
100 μl ($399)

APPLICATION

Application Note

*Optimal dilutions/concentrations should be determined by the researcher.
Application Recommended Dilution
WB 1:400
Not tested in other applications.

Calculated MW

76 kDa. ( Note )

Positive Control

Jurkat

PROPERTIES

Form

Liquid

Buffer

PBS, 1% BSA

Preservative

15mM Sodium azide

Storage

Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.

Concentration

Batch dependent (Please refer to the vial label for the specific concentration.)

Antigen Species

Human

Immunogen

synthetic peptide corresponding to the C-terminal region of human RIP (amino acids 634-650), conjugated to KLH.

Purification

Purified by affinity chromatography

Conjugation

Unconjugated

Note

For laboratory research use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.

Purchasers shall not, and agree not to enable third parties to, analyze, copy, reverse engineer or otherwise attempt to determine the structure or sequence of the product.

TARGET

Synonyms

receptor interacting serine/threonine kinase 1 , IMD57 , RIP , RIP-1 , RIP1

Cellular Localization

Cytoplasm,Cell membrane

Background

RIP (Receptor Interacting Protein) is a 74 kD Ser/Thr kinase which interacts with CD95 (Fas/APO1) receptor and the tumor necrosis factor receptor (TNFR1). It is a cell death domain adapter protein which can bind to the adapter proteins TRADD, RAID (CRADD) and TRAF2. RIP contains an N-terminal region with homology to protein kinases, an intermediate domain capable of association with MAPKKK and a C-terminal region containing an intracellular death domain motif. RIP activates both p38 MAP Kinase and SAPK families.3 In-vitro, RIP induces apoptosis, as well as SAPK/JNK and NF-kB activation. NF-kB activation through TRADD, TRAF2 and RIP can be triggered also by DR3/APO3 upon activation with APO3/Tweak ligand.DR4 and DR5 also use FADD, TRADD, and RIP in their signal transduction pathways. RIP-deficient mice fail to thrive, displaying extensive apoptosis in both lymphoid and adipose tissues and dying at 1-3 days of age. RIP possesses kinase activity as it autophosphorylates itself on serine and threonine residues.

Database

Research Area

REFERENCE

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REVIEW

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SDS
PBS.pdf
Sodium Azide.pdf
Package List Price ($)
$ 399