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AB15282

Sigma-Aldrich

Anti-Cone Arrestin Antibody

Chemicon®, from rabbit

Synonim(y):

Anti-Arrestin-C

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About This Item

Kod UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41
klon:
polyclonal
application:
IHC
WB
reaktywność gatunkowa:
rat, mouse
metody:
immunohistochemistry: suitable (paraffin)
western blot: suitable
citations:
248

pochodzenie biologiczne

rabbit

Poziom jakości

forma przeciwciała

affinity isolated antibody

rodzaj przeciwciała

primary antibodies

klon

polyclonal

masa cząsteczkowa

antibody estimated mol wt ~46 kDa

oczyszczone przez

affinity chromatography

reaktywność gatunkowa

rat, mouse

producent / nazwa handlowa

Chemicon®

metody

immunohistochemistry: suitable (paraffin)
western blot: suitable

izotyp

IgG

numer dostępu NCBI

numer dostępu UniProt

Warunki transportu

wet ice

docelowa modyfikacja potranslacyjna

unmodified

informacje o genach

mouse ... Arr3(170735)
rat ... Arr3(171107)

Opis ogólny

Arrestin-C (UniProt: Q9EQP6; also known as Cone arrestin, cArr, Retinal cone arrestin-3) is encoded by the Arr3 gene (Gene ID: 170735) in murine species. Arrestins are a superfamily of multi-functional proteins that regulate signaling and trafficking of the majority of G-protein-coupled receptors (GPCRs), as well as sub-cellular localization and activity of many other signaling proteins. Arrestin-C, a disulfide-linked, homodimeric protein, is predominantly found in inner and outer segments, and the inner plexiform regions of the retina. It is expressed in cone photoreceptors and pinealocytes and may contribute to the shut-off mechanisms associated with high acuity color vision. Arrestin-C is an elongated two-domain molecule with overall fold and key inter-domain interactions that hold the free protein in the basal conformation similar to the other subtypes. Several structural elements are reported to contribute to arrestin binding. The C-terminal acidic region serves as a regulatory role in controlling arrestin binding selectivity toward the phosphorylated and activated form of a receptor. The basic N-terminal domain directly participates in receptor interaction and serves a regulatory role via intramolecular interaction with the C-terminal acidic region. Also, two centrally localized domains are directly involved in determining receptor binding specificity and selectivity. Mutations in ARR3 gene in humans have been linked to X-lined myopia 26 that is characterized by typical tigroid fundus changes commonly seen in early onset high myopia. (Ref.: Gurevich, VV., et al. (2018). Protein Cell. 9; 986-1003; Xiao, X., et al. (2016). Mol. Vis. 22; 1257-1266).

Specyficzność

This rabbit polyclonal antibody detects Arrestin-C. It targets an epitope within 12 amino acids from the C-terminal region.

Immunogen

Epitope: C-terminus
KLH-conjugated linear peptide corresponding to 12 amino acids from the C-terminal region of mouse Cone Arrestin.

Zastosowanie

Anti-Cone Arrestin , Cat. No. AB15282, is a rabbit polyclonal antibody that detects Arrestin-C and is tested for use in Western Blotting and Immunohistochemistry (Paraffin).
Research Category
Neuroscience
Research Sub Category
Sensory & PNS
Tested Applications Immunohistochemistry (Paraffin) Analysis: A 1:250 dilution from a representative lot detected Cone Arrestin in mouse cerebellum, rat retina, and mouse retina tissue sections. Note: Actual optimal working dilutions must be determined by end user as specimens, and experimental conditions may vary with the end user

Jakość

Evaluated by Western Blotting in Mouse Retina tissue lysate. Western Blotting Analysis: A 1:500 dilution of this antibody detected Arrestin-C in Mouse Retina tissue lysate.

Opis wartości docelowych

Target molecular weight ~50 kDa observed. 41.92 kDa calculated. Uncharacterized bands may be observed in some lysate(s).

Postać fizyczna

ImmunoAffinity Purified
Purified rabbit polyclonal antibody in buffer containing 0.02 M phosphate buffer, pH 7.6, 0.25 M NaCl, and 0.1% sodium azide.

Przechowywanie i stabilność

Recommended storage: +2°C to +8°C.

Inne uwagi

Concentration: Please refer to lot specific datasheet.

Informacje prawne

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Oświadczenie o zrzeczeniu się odpowiedzialności

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Kod klasy składowania

10 - Combustible liquids

Klasa zagrożenia wodnego (WGK)

WGK 2

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable


Certyfikaty analizy (CoA)

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Masz już ten produkt?

Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.

Odwiedź Bibliotekę dokumentów

Phospholipid flippase ATP8A2 is required for normal visual and auditory function and photoreceptor and spiral ganglion cell survival.
Coleman, JA; Zhu, X; Djajadi, HR; Molday, LL; Smith, RS; Libby, RT; John, SW; Molday, RS
Journal of Cell Science null
Susanne F Koch et al.
The Journal of clinical investigation, 125(9), 3704-3713 (2015-08-25)
Hereditary retinal degenerative diseases, such as retinitis pigmentosa (RP), are characterized by the progressive loss of rod photoreceptors followed by loss of cones. While retinal gene therapy clinical trials demonstrated temporary improvement in visual function, this approach has yet to
Sensitivity and kinetics of signal transmission at the first visual synapse differentially impact visually-guided behavior.
Sarria, I; Pahlberg, J; Cao, Y; Kolesnikov, AV; Kefalov, VJ; Sampath, AP; Martemyanov, KA
eLife null
Katharina Kranz et al.
PloS one, 8(2), e57163-e57163 (2013-03-08)
Retinitis pigmentosa (RP) relates to a group of hereditary neurodegenerative diseases of the retina. On the cellular level, RP results in the primary death of rod photoreceptors, caused by rod-specific mutations, followed by a secondary degeneration of genetically normal cones.
Mei Chen et al.
PloS one, 8(4), e61381-e61381 (2013-05-03)
Previous studies have shown that CCL2/CX3CR1 deficient mice on C57BL/6N background (with rd8 mutation) have an early onset (6 weeks) of spontaneous retinal degeneration. In this study, we generated CCL2(-/-)CX3CR1(GFP/GFP) mice on the C57BL/6J background. Retinal degeneration was not detected

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