HtrA3 Antibody | 56-993

HtrA3 Antibody | 56-993 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Rat

Homology: N/A

Immunogen: This HtrA3 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 112-144 amino acids from the N-terminal region of human HtrA3.

Research Area: Signal Transduction

Tested Application: WB, IHC-P

Application: For WB starting dilution is: 1:1000
For IHC-P starting dilution is: 1:50~100

Specificiy: N/A

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 49 kDa

Validation: N/A

Isoform: N/A

Purification: This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis

Clonality: Polyclonal

Clone: N/A

Isotype: Rabbit Ig

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.

Concentration: batch dependent

Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Alternate Name: Serine protease HTRA3, 3421-, High-temperature requirement factor A3, Pregnancy-related serine protease, HTRA3, PRSP

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

BACKGROUND: Insulin-like growth factors (IGFs) stimulate the proliferation and differentiation of a vast number of cell types. The action of the growth factors is mediated and controlled by a complex system of components, including several proteases that cleave the IGF-Binding Proteins. HtrA1 is a 480 aa protein that contains an N-terminus homologous to MAC25 (IGFBP7) with a conserved Kazal-type serine protease inhibitor motif, as well as a C-terminal PDZ domain. Semiquantitative RT-PCR and immunoblot analyses showed an approximately 7-fold increase of PRSS11 in osteoarthritis cartilage compared with controls. HTRA2 is released from mitochondria and inhibits the function of XIAP by direct binding in a way similar to SMAC. Moreover, when overexpressed extramitochondrially, HTRA2 induced atypical cell death, which was neither accompanied by a significant increase in caspase activity nor inhibited by caspase inhibitors, including XIAP. A catalytically inactive mutant of HTRA2, however, did not induce cell death. Suzuki et al. (2001) concluded that HTRA2 is a SMAC-like inhibitor of IAP (inhibitor of apoptosis proteins) activity with a serine protease-dependent cell death-inducing activity.