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N-alpha-acetylation is among the most common post-translational protein modifications in eukaryotic cells. 再加上，我们可以发ARD1 Homolog, N-Acetyltransferase 蛋白 (9) 和 ARD1 Homolog, N-Acetyltransferase 试剂盒 (3)和数多这个蛋白质的别的产品。
Showing 10 out of 51 products:
Human Polyclonal ARD1A Primary Antibody for ELISA - ABIN563573
Azizi, Li, Ströbel, Chen, Slavc, Lubec: Identification of c-myc-dependent proteins in the medulloblastoma cell line D425Med. in Amino acids 2012
Human Polyclonal ARD1A Primary Antibody for ICC, IF - ABIN4337709
Simsek, Tiu, Flynn, Byeon, Leppek, Xu, Chang, Barna: The Mammalian Ribo-interactome Reveals Ribosome Functional Diversity and Heterogeneity. in Cell 2017
In combination with acetylation assays, the HypK N-terminal region is identified as a negative regulator of the NatA acetylation activity
ARD1 (显示 TRIM23 抗体)-mediated Hsp70 (显示 HSP70 抗体) acetylation is a regulatory mechanism that temporally balances protein refolding/degradation in response to stress
Negative regulation of Naa10 towards NTN1 (显示 NTN1 抗体) and its receptor UNC5B (显示 UNC5B 抗体) were also detected upon treatment of all-trans retinoid acid, which was often used to induce morphological differentiation.
A novel de novo NAA10 c.332 T>G p.(Val111Gly) missense variant was detected in a girl with mild/moderate non-syndromic intellectual disability. NAA10 V111G displayed reduced monomeric NAT (显示 BRD2 抗体) activity and stability, but intact NatA-mediated NAT (显示 BRD2 抗体) activity.
Expression of ARD1 (显示 TRIM23 抗体) increases levels of androgen receptor (显示 AR 抗体) acetylation and androgen receptor (显示 AR 抗体)-HSP90 (显示 HSP90 抗体) dissociation in a dose dependent manner.
Study reports on a total of 12 affected females with four different de novo missense mutations in NAA10 and one inherited mutation in a familial case due to germline mosaicism, thus further expanding themutational and clinical spectrum associated with NAA10 related N-terminal-acetyltransferase (显示 NAA15 抗体) deficiency.
The results observed an inverse correlation between the expression of NAA10 and that of miR (显示 MLXIP 抗体)-342-5p and miR (显示 MLXIP 抗体)-608 .
Human Naa15 (NATH (显示 NAA15 抗体)) and Naa10 (ARD1) form a stable NatA complex which associates with ribosomes and performs co-translational N-terminal acetylation; Naa15 (NATH (显示 NAA15 抗体)) and Naa10 (ARD1) are cleaved during apoptosis resulting in decreased acetyltransferase activity
The clinical spectrum of NAA10.
there is no difference in lysine acetylation of substrate proteins with or without Naa10, suggesting that the substrates may be acetylated chemically rather than enzymatically.
The lethal Ogden syndrome-associated mutation of Naa10p disrupts its binding to the imprinting control region of H19 (显示 NCKAP1 抗体) and Dnmt1 (显示 DNMT1 抗体) recruitment.
NAA10 acts as a guard ensuring balanced osteogenesis by fine-tuning Runx2 (显示 RUNX2 抗体) signalling in a feedback manner.
ARD1 has a crucial role in the cellular response to oxidative stress as a bona fide regulator of MSRA (显示 MSR1 抗体).
mARD1A(225) may be a novel upstream target that blocks VEGFA (显示 VEGFA 抗体) expression and tumor-related angiogenesis.
Biochemical analysis demonstrated that mNAT1 and its evolutionarily conserved co-subunit, mARD1, assemble to form a functional acetyltransferase.
Mouse ortholog (225) of ARD1 strongly decreased the level of hypoxia inducible factor (HIF)-1 alpha (显示 HIF1A 抗体) and increased the extent of acetylation, whereas mARD1(235) variants had a much weaker effect on HIF-1 alpha (显示 HIF1A 抗体) stability and acetylation.
These results indicate that ARD1(235) and ARD1(225) isoforms may have different activities and function in different subcellular compartments of mammalian cells.
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 normal cell function. This gene encodes an N-terminal acetyltransferase that functions as the catalytic subunit of the major amino-terminal acetyltransferase A complex. Mutations in this gene are the cause of Ogden syndrome. Alternate splicing results in multiple transcript variants.
ARD1 homolog A, N-acetyltransferase
, N-acetyltransferase ARD1, human homolog of
, N-alpha-acetyltransferase 10
, N-alpha-acetyltransferase 10, NatA catalytic subunit
, N-terminal acetyltransferase complex ARD1 subunit homolog A
, alpha-N-acetyltransferase 1A
, natA catalytic subunit
, N-acetyltransferase ARD1
, N(alpha)-acetyltransferase 10, NatA catalytic subunitNalpha acetyltransferase 10
, N-acetyltransferase ARD1 homolog
, Nalpha acetyltransferase 10