ARD1A Blocking Peptide
- Known as:
- ARD1A Blocking Peptide
- Catalog number:
- 33r-9510
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- ARD1A Blocking Peptide
Related genes to: ARD1A Blocking Peptide
- Gene:
- NAA10 NIH gene
- Name:
- N(alpha)-acetyltransferase 10, NatA catalytic subunit
- Previous symbol:
- ARD1, ARD1A
- Synonyms:
- DXS707, TE2
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-29
- Date modifiied:
- 2017-12-15
Related products to: ARD1A Blocking Peptide
Related articles to: ARD1A Blocking Peptide
- Diabetic kidney disease (DKD) is a frequent complication associated with diabetes. CREBRF was reported to be closely associated with endoplasmic reticulum stress. However, the upstream regulatory mechanism by which CREBRF modulates endoplasmic reticulum stress in DKD renal tubular injury is unknown. - Source: PubMed
Publication date: 2026/06/09
Fang SitianNing JingHuang JinjingChen Yanxia - Human dental pulp stem cells (hDPSCs) hold great promise for dental tissue regeneration, yet the molecular mechanisms underlying their odontogenic differentiation remain unclear. This study investigates the role of nucleoside diphosphate kinase 3 (NME3) in regulating hDPSC differentiation. NME3 was found to be specifically expressed in odontoblasts of rat tooth germs and positively associated with odontogenic markers (DSPP, DMP1, and RUNX2) in hDPSCs. Functional assays revealed that NME3 promotes odontogenic differentiation, while its knockdown suppresses mineralization and marker expression. Mass spectrometry identified N-α-acetyltransferase 10 (NAA10) as a potential NME3-interacting protein, with both showing colocalization in hDPSCs and developing odontoblasts. Mechanistically, NAA10 knockdown rescued the differentiation deficits caused by NME3 silencing, and NAA10 overexpression attenuated the effects of NME3. Moreover, NME3 appears to facilitate the nuclear translocation of RUNX2, a key transcription factor in odontogenesis. These findings suggest that NME3 may regulate hDPSC odontogenic differentiation through interaction with NAA10 and modulation of RUNX2 localization, offering new insights into the molecular control of dental tissue regeneration. - Source: PubMed
Fan ChangxiuXu KeFei WenchaoLi YuejunZhao ShouliangJu Yanqin - Childhood interstitial lung diseases (chILDs) are rare, heterogeneous chronic pulmonary disorders that are often underdiagnosed due to their low prevalence and nonspecific clinical presentation. Persistent tachypnea of infancy, often referred to as neuroendocrine cell hyperplasia of infancy (PTI/NEHI), is one of the most frequent forms of chILD, although its underlying etiology remains unknown. - Source: PubMed
Publication date: 2026/05/14
Rapp Christina KMauss-Schwarzer KatharinaKappler MatthiasPawlita IngoDillenhoefer StefanieWiemers AnnaMarczak HonorataKrenke KatarzynaLange JoannaEschenhagen Patience NWarfsmann JulianMiranda LucasMueller-Myhsok BertramMueller-Reif Johannes BNathan SuzanneHaemmerling SusanneSchwerk NicolausStehling FlorianGriese Matthias - Cellular metabolism is precisely regulated in response to nutrient availability. As an extremely energy-consuming anabolic process, ribosome biogenesis should be tightly controlled in response to nutrient supply. However, how the nucleolus responds to different nutrient statuses remains poorly understood. Here, we show that C7orf50 is a nucleolus-localized protein and functions as a coordinator between ribosome biogenesis and autophagy, acting as what we term a "nutrient-responding nucleolar factor." C7orf50 undergoes reversible nucleolus-nucleoplasm translocation in response to nutrient deprivation and supply, with its nucleolus and nucleoplasm location dictating ribosome biogenesis and autophagic augmentation, respectively. The location-dependent function of C7orf50 is determined by acetylation at the lysine-71/lysine-72/lysine-76 residues by N-alpha-acetyltransferase 10, a substrate of mammalian target of rapamycin and a nutritional status-responsive acetyltransferase. In vivo and in vitro assays show that C7orf50 acts as an oncoprotein that promotes tumor growth. Our findings reveal a nucleolus-localized coordinating mechanism for the regulation of anabolism and catabolism transition by nutrient status. - Source: PubMed
Publication date: 2026/05/15
Sun JingyuYang MeiLi QianLiang JiaweiFeng HaipingGao LijieWang YunLiu HongmeiGuo CaixiaTang Tie-Shan - A girl had been seen at 15 months of age for developmental expressive language and gross motor delays and had subsequent serially normal neurological evaluations until age 6 years when she developed a new abnormality of gait clinically similar to a paroxysmal kinesigenic dyskinesia for which she tested negative. Multiple maternal family members were known to have a pathogenetic variant in N-α-acetyltransferase 10 (NAA10) [c.235C>T (p.R79C)]. The appearance of a gait disorder in association with NAA10-related syndrome has not been previously described and expands the phenotype of this disorder to include this novel neurological symptom. The relevant literature of the very few cases of NAA10-related syndrome that include passing mention of any movement or gait abnormality is reviewed. - Source: PubMed
Publication date: 2026/05/14
Brown William D