PACT (PKR activating protein) / PRKRA Antibody (Rabbit mAb) [E15C21] Datasheet

Biological Description

Specificity	PACT Antibody (Rabbit mAb) [E15C21] detects endogenous levels of total PACT protein.
Background	PACT belongs to the family of double-stranded RNA-binding proteins that regulate innate immune and stress-response signaling through direct protein-protein interactions rather than enzymatic activity of their own, and it carries tandem double-stranded RNA-binding motifs that mediate its engagement with multiple partner proteins. PACT functions as a direct cellular activator of protein kinase R, engaging PKR independently of viral double-stranded RNA and instead responding to cellular stress signals such as serum starvation and oxidative insult; this interaction triggers PKR autophosphorylation and subsequent phosphorylation of eIF2α, producing a transient attenuation of global protein synthesis as part of the integrated stress response, and sustained or dysregulated signaling through this axis can shift the pathway from a protective outcome toward apoptosis. Beyond PKR activation, PACT associates with the RNA interference machinery, forming a complex with Dicer and Argonaute2 that supports processing of small interfering RNA and influences the efficiency of microRNA accumulation, linking a single dsRNA-binding scaffold to both translational control and post-transcriptional gene silencing. PACT additionally binds directly to the C-terminal repression domain of RIG-I, a cytosolic viral RNA sensor, and this interaction stimulates the ATPase activity of RIG-I and potentiates RIG-I-driven type I interferon production independently of PKR or Dicer engagement, extending PACT's regulatory reach into antiviral innate immune signaling and positioning it as a convergence point across three distinct pathways. Physiological roles for PACT extend to development, since loss of the murine ortholog produces craniofacial and pituitary developmental defects alongside fertility impairment, indicating functions beyond acute stress signaling. Mutations in the gene encoding PACT are linked to dystonia, a movement disorder featuring involuntary muscle contractions, and disease-associated variants alter dsRNA-binding capacity and disrupt normal PKR regulation, producing dysregulated eIF2α signaling and a compromised stress response in affected cells.

Specificity

PACT Antibody (Rabbit mAb) [E15C21] detects endogenous levels of total PACT protein.

Background

PACT belongs to the family of double-stranded RNA-binding proteins that regulate innate immune and stress-response signaling through direct protein-protein interactions rather than enzymatic activity of their own, and it carries tandem double-stranded RNA-binding motifs that mediate its engagement with multiple partner proteins. PACT functions as a direct cellular activator of protein kinase R, engaging PKR independently of viral double-stranded RNA and instead responding to cellular stress signals such as serum starvation and oxidative insult; this interaction triggers PKR autophosphorylation and subsequent phosphorylation of eIF2α, producing a transient attenuation of global protein synthesis as part of the integrated stress response, and sustained or dysregulated signaling through this axis can shift the pathway from a protective outcome toward apoptosis. Beyond PKR activation, PACT associates with the RNA interference machinery, forming a complex with Dicer and Argonaute2 that supports processing of small interfering RNA and influences the efficiency of microRNA accumulation, linking a single dsRNA-binding scaffold to both translational control and post-transcriptional gene silencing. PACT additionally binds directly to the C-terminal repression domain of RIG-I, a cytosolic viral RNA sensor, and this interaction stimulates the ATPase activity of RIG-I and potentiates RIG-I-driven type I interferon production independently of PKR or Dicer engagement, extending PACT's regulatory reach into antiviral innate immune signaling and positioning it as a convergence point across three distinct pathways. Physiological roles for PACT extend to development, since loss of the murine ortholog produces craniofacial and pituitary developmental defects alongside fertility impairment, indicating functions beyond acute stress signaling. Mutations in the gene encoding PACT are linked to dystonia, a movement disorder featuring involuntary muscle contractions, and disease-associated variants alter dsRNA-binding capacity and disrupt normal PKR regulation, producing dysregulated eIF2α signaling and a compromised stress response in affected cells.

Usage Information

Application

WB, IP

Dilution

WB	IP
1:1000	1:50

Reactivity

Human, Monkey

Source

Rabbit Monoclonal Antibody

MW

30 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

References

https://pubmed.ncbi.nlm.nih.gov/25554729/
https://pubmed.ncbi.nlm.nih.gov/21501829/

PACT (PKR activating protein) / PRKRA Antibody (Rabbit mAb) [E15C21]

Biological Description

Usage Information

References

Application Data