Datasheet

生物学的記述

Specificity	Coronin 1a/TACO Antibody (Rabbit mAb) [N18B9] detects endogenous levels of total Coronin 1a/TACO protein.
Background	Coronin 1A, also known as TACO, is a leukocyte-enriched actin-binding WD40-repeat protein of the coronin family that localizes to the cortical cytoskeleton and phagosomal membranes and functions as a regulator of actin dynamics, membrane trafficking and Ca²⁺-dependent signaling during immune responses and host–pathogen interactions. The protein contains an N‑terminal β‑propeller formed by WD repeats that binds F‑actin and Arp2/3, a more variable central region, and a C‑terminal coiled-coil segment implicated in oligomerization and interactions with signaling partners, allowing coronin 1A to bridge adjacent actin protomers and stabilize F‑actin while coordinating actin-remodeling factors at sites of membrane invagination and protrusion. Coronin 1A binds along actin filaments in a manner that can both stabilize filament bundles and modulate access of ADF/cofilin and Arp2/3, placing it as a hub that tunes leading-edge actin assembly, immunological synapse formation and motile behavior in hematopoietic cells. In T lymphocytes, coronin 1A links cytoskeleton plasticity to TCRαβ-induced signaling: loss of coronin 1A results in defective terminal development and survival of αβ T cells, excessive accumulation but reduced dynamics of F‑actin and WASP–Arp2/3 components at the immunological synapse, prolonged cell–cell contact, and impaired TCR signaling characterized by elevated basal JNK activation, reduced TCR-induced Ca²⁺ influx and defective IκB phosphorylation and degradation, indicating that coronin 1A is required to couple actin remodeling with proper engagement of Ca²⁺ and NF‑κB pathways. These defects translate into altered cytokine production and homeostasis of naïve T cells, and coronin 1A is a key factor in maintaining naïve T-cell survival and migration in response to chemokine cues, with recessive CORO1A mutations producing peripheral T-cell deficiency due to migration defects and increased apoptosis. In macrophages, coronin 1A/TACO plays a specialized role during mycobacterial infection: pathogenic mycobacteria recruit coronin 1A to the phagosomal membrane, where its continued presence prevents phagosome–lysosome fusion and allows bacilli to persist within nonacidified compartments. Coronin 1A is dispensable for general F‑actin-dependent processes such as phagocytosis, motility and membrane ruffling, but is required for activation of the Ca²⁺-dependent phosphatase calcineurin upon mycobacterial infection; in its absence, calcineurin activation fails, phagosomes proceed to lysosomal fusion and mycobacteria are killed, and pharmacologic inhibition of calcineurin similarly restores lysosomal delivery, defining a coronin 1A–calcineurin axis that specifically controls phagosome maturation in infected cells. Coronin 1A also modulates Rac1 signaling during cell migration by promoting a cytoskeletal-based feedback loop in which Rac1 activation drives actin remodeling that, in turn, maintains Rac1 at membranes and supports persistent motility, further integrating coronin 1A into Rho-family GTPase pathways that coordinate cell shape and movement. Coronin 1A also regulates lysosomal secretion in osteoclast-lineage cells, where it acts as a negative regulator of cathepsin K exocytosis and bone resorption by interfering with LC3 lipidation at the ruffled border and limiting lysosome–plasma membrane fusion in an actin-dependent fashion.

Specificity

Coronin 1a/TACO Antibody (Rabbit mAb) [N18B9] detects endogenous levels of total Coronin 1a/TACO protein.

Background

Coronin 1A, also known as TACO, is a leukocyte-enriched actin-binding WD40-repeat protein of the coronin family that localizes to the cortical cytoskeleton and phagosomal membranes and functions as a regulator of actin dynamics, membrane trafficking and Ca²⁺-dependent signaling during immune responses and host–pathogen interactions. The protein contains an N‑terminal β‑propeller formed by WD repeats that binds F‑actin and Arp2/3, a more variable central region, and a C‑terminal coiled-coil segment implicated in oligomerization and interactions with signaling partners, allowing coronin 1A to bridge adjacent actin protomers and stabilize F‑actin while coordinating actin-remodeling factors at sites of membrane invagination and protrusion. Coronin 1A binds along actin filaments in a manner that can both stabilize filament bundles and modulate access of ADF/cofilin and Arp2/3, placing it as a hub that tunes leading-edge actin assembly, immunological synapse formation and motile behavior in hematopoietic cells. In T lymphocytes, coronin 1A links cytoskeleton plasticity to TCRαβ-induced signaling: loss of coronin 1A results in defective terminal development and survival of αβ T cells, excessive accumulation but reduced dynamics of F‑actin and WASP–Arp2/3 components at the immunological synapse, prolonged cell–cell contact, and impaired TCR signaling characterized by elevated basal JNK activation, reduced TCR-induced Ca²⁺ influx and defective IκB phosphorylation and degradation, indicating that coronin 1A is required to couple actin remodeling with proper engagement of Ca²⁺ and NF‑κB pathways. These defects translate into altered cytokine production and homeostasis of naïve T cells, and coronin 1A is a key factor in maintaining naïve T-cell survival and migration in response to chemokine cues, with recessive CORO1A mutations producing peripheral T-cell deficiency due to migration defects and increased apoptosis. In macrophages, coronin 1A/TACO plays a specialized role during mycobacterial infection: pathogenic mycobacteria recruit coronin 1A to the phagosomal membrane, where its continued presence prevents phagosome–lysosome fusion and allows bacilli to persist within nonacidified compartments. Coronin 1A is dispensable for general F‑actin-dependent processes such as phagocytosis, motility and membrane ruffling, but is required for activation of the Ca²⁺-dependent phosphatase calcineurin upon mycobacterial infection; in its absence, calcineurin activation fails, phagosomes proceed to lysosomal fusion and mycobacteria are killed, and pharmacologic inhibition of calcineurin similarly restores lysosomal delivery, defining a coronin 1A–calcineurin axis that specifically controls phagosome maturation in infected cells. Coronin 1A also modulates Rac1 signaling during cell migration by promoting a cytoskeletal-based feedback loop in which Rac1 activation drives actin remodeling that, in turn, maintains Rac1 at membranes and supports persistent motility, further integrating coronin 1A into Rho-family GTPase pathways that coordinate cell shape and movement. Coronin 1A also regulates lysosomal secretion in osteoclast-lineage cells, where it acts as a negative regulator of cathepsin K exocytosis and bone resorption by interfering with LC3 lipidation at the ruffled border and limiting lysosome–plasma membrane fusion in an actin-dependent fashion.

使用情報

Application

WB, IHC, IF, FCM

Dilution

WB	IHC	IF	FCM
1:1000	1:1000	1:100	1:500

Reactivity

Mouse, Rat, Human

Source

Rabbit Monoclonal Antibody

MW

51 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

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/17632055/
https://pubmed.ncbi.nlm.nih.gov/18941544/

Coronin 1a/TACO Antibody (Rabbit mAb) [N18B9]

生物学的記述

使用情報

References

Application Data