Datasheet

Biological Description

Specificity	Anti-Rac1 Mouse Antibody [D22N1] recognizes endogenous levels of total Rac1 protein.
Background	Ras-related C3 botulinum toxin substrate 1 (Rac1) is a small GTPase belonging to the Rac subfamily of the Rho family, widely recognized for its role in cytoskeletal regulation and control of gene expression. Rac1 participates in numerous cellular processes, including cell plasticity, migration, invasion, adhesion, proliferation, apoptosis, production of reactive oxygen species (ROS), and regulation of inflammatory responses—all of which are essential for normal physiology. Disruption of Rac1 signaling can drive disease, as many Rac1-regulated pathways contribute to pathological conditions such as cancer, cardiovascular and kidney diseases, neurodegenerative disorders, aberrant inflammation, and infections. Functionally, Rac1 cycles between an inactive GDP-bound state and an active GTP-bound state. This switch is tightly controlled by guanine nucleotide exchange factors (GEFs), which promote GDP-GTP exchange; GTPase-activating proteins (GAPs), which accelerate GTP hydrolysis; and Rho guanine nucleotide dissociation inhibitors (RhoGDIs), which stabilize the inactive form. In addition to nucleotide cycling, Rac1 activity, stability, and subcellular localization are further regulated through diverse post-translational modifications, ensuring precise spatial and temporal control of Rac1 signaling.

Specificity

Anti-Rac1 Mouse Antibody [D22N1] recognizes endogenous levels of total Rac1 protein.

Background

Ras-related C3 botulinum toxin substrate 1 (Rac1) is a small GTPase belonging to the Rac subfamily of the Rho family, widely recognized for its role in cytoskeletal regulation and control of gene expression. Rac1 participates in numerous cellular processes, including cell plasticity, migration, invasion, adhesion, proliferation, apoptosis, production of reactive oxygen species (ROS), and regulation of inflammatory responses—all of which are essential for normal physiology. Disruption of Rac1 signaling can drive disease, as many Rac1-regulated pathways contribute to pathological conditions such as cancer, cardiovascular and kidney diseases, neurodegenerative disorders, aberrant inflammation, and infections. Functionally, Rac1 cycles between an inactive GDP-bound state and an active GTP-bound state. This switch is tightly controlled by guanine nucleotide exchange factors (GEFs), which promote GDP-GTP exchange; GTPase-activating proteins (GAPs), which accelerate GTP hydrolysis; and Rho guanine nucleotide dissociation inhibitors (RhoGDIs), which stabilize the inactive form. In addition to nucleotide cycling, Rac1 activity, stability, and subcellular localization are further regulated through diverse post-translational modifications, ensuring precise spatial and temporal control of Rac1 signaling.

Usage Information

Application

WB, IP, IHC

Dilution

WB

1:1000

Reactivity

Mouse, Rat, Human

Source

Mouse

MW

21 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

Exprimental Methods

References

https://pubmed.ncbi.nlm.nih.gov/27442895/

Anti-Rac1 Mouse Antibody [D22N1]

Biological Description

Usage Information

References

Application Data