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Merck
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Key Documents

SAB2108642

Sigma-Aldrich

Anti-ACTN2 Antibody

rabbit polyclonal

Sinónimos:

Anti-CMD1AA

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

product name

Anti-ACTN2, affinity isolated antibody

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

104 kDa

species reactivity

rabbit, rat, mouse, human, guinea pig

concentration

0.5-1 mg/mL

technique(s)

immunoblotting: suitable
immunohistochemistry: suitable

accession no.

NM_001103

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... ACTN2(88)

Immunogen

Synthetic peptide directed towards the N terminal region of human ACTN2

Biochem/physiol Actions

The alpha-actinins are a multigene family of four actin-binding proteins related to dystrophin. The two skeletal muscle isoforms of alpha-actinin (ACTN2 and ACTN3) are major structural components of the Z-line involved in anchoring the actin-containing thin filaments. In humans, ACTN2 is expressed in all muscle fibres, while ACTN3 expression is restricted to a subset of type 2 fibres. Murine Actn2 and Actn3 are differentially expressed, spatially and temporally, during embryonic development and, in contrast to humans, alpha-actinin-2 expression does not completely overlap alpha-actinin-3 in postnatal skeletal muscle, suggesting independent function.Alpha actinins belong to the spectrin gene superfamily which represents a diverse group of cytoskeletal proteins, including the alpha and beta spectrins and dystrophins. Alpha actinin is an actin-binding protein with multiple roles in different cell types. In nonmuscle cells, the cytoskeletal isoform is found along microfilament bundles and adherens-type junctions, where it is involved in binding actin to the membrane. In contrast, skeletal, cardiac, and smooth muscle isoforms are localized to the Z-disc and analogous dense bodies, where they help anchor the myofibrillar actin filaments. This gene encodes a muscle-specific, alpha actinin isoform that is expressed in both skeletal and cardiac muscles. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Entrez Gene record to access additional publications. PRIMARYREFSEQ_SPAN PRIMARY_IDENTIFIER PRIMARY_SPAN COMP 1-39 DC378038.1 17-55 40-2961 BC051770.1 1-2922 2962-3458 CB153006.1 65-561 3459-3637 AL359185.25 28531-28709 3638-4210 M86406.1 3609-4181 4211-4528 AL359185.25 29283-29600

Sequence

Synthetic peptide located within the following region: NQIEPGVQYNYVYDEDEYMIQEEEWDRDLLLDPAWEKQQRKTFTAWCNSH

Physical form

Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

Disclaimer

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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Storage Class

10 - Combustible liquids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Simon Diering et al.
The Journal of biological chemistry, 295(45), 15342-15365 (2020-09-02)
The contraction and relaxation of the heart is controlled by stimulation of the β1-adrenoreceptor (AR) signaling cascade, which leads to activation of cAMP-dependent protein kinase (PKA) and subsequent cardiac protein phosphorylation. Phosphorylation is counteracted by the main cardiac protein phosphatases
Maksymilian Prondzynski et al.
EMBO molecular medicine, 11(12), e11115-e11115 (2019-11-05)
Hypertrophic cardiomyopathy (HCM) is a cardiac genetic disease accompanied by structural and contractile alterations. We identified a rare c.740C>T (p.T247M) mutation in ACTN2, encoding α-actinin 2 in a HCM patient, who presented with left ventricular hypertrophy, outflow tract obstruction, and

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