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Mouse Anti-NAA10 Recombinant Antibody (CBYC-A1003) (CBMAB-A4591-YC)

Provided herein is a Mouse monoclonal antibody against Human N(Alpha)-Acetyltransferase 10, NatA Catalytic Subunit. The antibody can be used for immunoassay techniques, such as IF.
See all NAA10 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBYC-A1003
Antibody Isotype
IgG
Application
IF

Basic Information

Specificity
Human
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
N(Alpha)-Acetyltransferase 10, NatA Catalytic Subunit
Introduction
N-alpha-acetylation is among the most common post-translational protein modifications in eukaryotic cells. This process involves the transfer of an acetyl group from acetyl-coenzyme A to the alpha-amino group on a nascent polypeptide and is essential for
Entrez Gene ID
8260
UniProt ID
P41227
Alternative Names
ARD1P; DXS707; ARD1; OGDNS; ARD1A; TE2; MCOPS1; NATD
Function
Catalytic subunit of N-terminal acetyltransferase complexes which display alpha (N-terminal) acetyltransferase activity (PubMed:15496142, PubMed:19826488, PubMed:19420222, PubMed:20145209, PubMed:27708256, PubMed:25489052, PubMed:29754825, PubMed:20154145, PubMed:32042062).

Acetylates amino termini that are devoid of initiator methionine (PubMed:19420222).

The alpha (N-terminal) acetyltransferase activity may be important for vascular, hematopoietic and neuronal growth and development. Without NAA15, displays epsilon (internal) acetyltransferase activity towards HIF1A, thereby promoting its degradation (PubMed:12464182).

Represses MYLK kinase activity by acetylation, and thus represses tumor cell migration (PubMed:19826488).

Acetylates, and stabilizes TSC2, thereby repressing mTOR activity and suppressing cancer development (PubMed:20145209).

Acetylates HSPA1A and HSPA1B at 'Lys-77' which enhances its chaperone activity and leads to preferential binding to co-chaperone HOPX (PubMed:27708256).

Acetylates HIST1H4A (PubMed:29754825).

Acts as a negative regulator of sister chromatid cohesion during mitosis (PubMed:27422821).
Biological Process
DNA packaging Source: ProtInc
Internal protein amino acid acetylation Source: ProtInc
Negative regulation of maintenance of mitotic sister chromatid cohesion, centromeric Source: UniProtKB
N-terminal peptidyl-glutamic acid acetylation Source: GO_Central
N-terminal peptidyl-serine acetylation Source: GO_Central
N-terminal protein amino acid acetylation Source: UniProtKB
Protein acetylation Source: UniProtKB
Cellular Location
Cytoplasm
Nucleus
Note: Also present in the free cytosolic and cytoskeleton-bound polysomes.
Involvement in disease
N-terminal acetyltransferase deficiency (NATD):
An enzymatic deficiency resulting in postnatal growth failure with severe delays and dysmorphic features. It is clinically characterized by wrinkled forehead, prominent eyes, widely opened anterior and posterior fontanels, downsloping palpebral fissures, thickened lids, large ears, flared nares, hypoplastic alae, short columella, protruding upper lip, and microretrognathia. There are also delayed closing of fontanels and broad great toes. Skin is characterized by redundancy or laxity with minimal subcutaneous fat, cutaneous capillary malformations, and very fine hair and eyebrows. Death results from cardiogenic shock following arrhythmia.
Microphthalmia, syndromic, 1 (MCOPS1):
A rare syndrome defined by the canonical features of unilateral or bilateral microphthalmia or anophthalmia and defects in the skeletal and genitourinary systems. Microphthalmia is a disorder of eye formation, ranging from small size of a single eye to complete bilateral absence of ocular tissues (anophthalmia). In many cases, microphthalmia/anophthalmia occurs in association with syndromes that include non-ocular abnormalities. Anomalies of the digits, teeth, and ears are hallmarks of MCOPS1. Intellectual disability ranges from mild to severe, with self-mutilating behaviors and seizures in severely affected MCOPS1 individuals.
PTM
Cleaved by caspases during apoptosis.
Phosphorylation by IKBKB/IKKB at Ser-209 promotes its proteasome-mediated degradation.
Autoacetylated at Lys-136 which stimulates its catalytic activity.
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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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