PSTPIP1 Antibody | 23-164

PSTPIP1 Antibody | 23-164 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse, Rat

Homology: N/A

Immunogen: Recombinant fusion protein containing a sequence corresponding to amino acids 157-416 of human PSTPIP1 (NP_003969.2) .

Research Area: Cell Cycle, Signal Transduction

Tested Application: WB, IHC

Application: WB: 1:500 - 1:2000
IHC: 1:50 - 1:200

Specificiy: N/A

Positive Control 1: THP-1

Positive Control 2: mouse spleen

Positive Control 3: mouse thymus

Positive Control 4: mouse brain

Positive Control 5: rat brain

Positive Control 6: Mouse spleen

Molecular Weight: Observed: 48kDa

Validation: N/A

Isoform: N/A

Purification: Affinity purification

Clonality: Polyclonal

Clone: N/A

Isotype: IgG

Conjugate: Unconjugated

Physical State: Liquid

Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.

Concentration: N/A

Storage Condition: Store at -20˚C. Avoid freeze / thaw cycles.

Alternate Name: Proline-serine-threonine phosphatase-interacting protein 1, PEST phosphatase-interacting protein 1, CD2-binding protein 1, H-PIP, PSTPIP1, CD2BP1

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: This gene encodes a cytoskeletal protein that is highly expressed in hemopoietic tissues. This protein functions via its interaction with several different proteins involved in cytoskeletal organization and inflammatory processes. It binds to the cytoplasmic tail of CD2, an effector of T cell activation and adhesion, downregulating CD2-triggered adhesion. It binds PEST-type protein tyrosine phosphatases (PTP) and directs them to c-Abl kinase to mediate c-Abl dephosphorylation, thereby, regulating c-Abl activity. It also interacts with pyrin, which is found in association with the cytoskeleton in myeloid/monocytic cells and modulates immunoregulatory functions. Mutations in this gene are associated with PAPA (pyogenic sterile arthritis, pyoderma gangrenosum, and acne) syndrome. It is hypothesized that the disease-causing mutations compromise physiologic signaling necessary for the maintenance of a proper inflammatory response.