TRIM29 antibody - middle region (ARP32521_P050)
- Known as:
- TRIM29 (anti-) - middle region (ARP32521_P050)
- Catalog number:
- arp32521_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TRIM29 antibody - middle region (ARP32521_P050)
Related genes to: TRIM29 antibody - middle region (ARP32521_P050)
- Gene:
- TRIM29 NIH gene
- Name:
- tripartite motif containing 29
- Previous symbol:
- -
- Synonyms:
- ATDC, FLJ36085
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-28
- Date modifiied:
- 2014-11-18
Related products to: TRIM29 antibody - middle region (ARP32521_P050)
Related articles to: TRIM29 antibody - middle region (ARP32521_P050)
- Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, concerning the cell migration and invasion assay experiments in Fig. 2C and D on p. 8248, a number of data panels contained overlapping sections, such that data which were shown to represent different experimental conditions had been derived from a smaller number of original sources. Given the time that has elapsed since this paper was published, the authors no longer had access to their original data, but were willing to repeat these experiments, and the revised version of Fig. 2 is shown on the next page. The results obtained were broadly similar to those obtained originally, and therefore the replacement of the original data in this figure with the new data does not affect the reported conclusions of this study. All the authors agree with the publication of this Corrigendum, and are grateful to the Editor of for allowing this to be published. They also regret the errors that existed in the original figure, and apologize to the readership for any confusion that may have been caused. [Molecular Medicine Reports 17: 8244-8252, 2018; DOI: 10.3892/mmr.2018.8894]. - Source: PubMed
Publication date: 2026/04/17
Yang YanLi QingGuo Lili - - Source: PubMed
Publication date: 2026/04/10
Zhou XuanyuJia WeikunJiang HequnZhong HuafeiSun JieMa RuidongWu ZhiqiangLin ZhiwuLu LingChen Hu - - Source: PubMed
Publication date: 2026/04/09
Liu LongGao ZhenzhenWang QiZhao XiaohongZhang FabiaoZhu YuSun WangyangHuang YuxiWang ZhenboYan ShengLi ShaoweiZhang Yu - Chondrocyte senescence accelerates osteoarthritis (OA) progression, with dysregulated glycolysis potentially driving this process through lactate accumulation and histone lactylation. However, the mechanistic connection between lactate-induced lactylation and cellular senescence in OA chondrocytes remains poorly understood. This study elucidates this relationship and explores its therapeutic relevance. Using clinical OA cartilage, animal models, and IL-1β-stimulated chondrocytes, we demonstrated enhanced glycolysis and senescence activities. Increased glycolytic activity and lactate accumulation promoted cellular senescence in the OA microenvironment. Elevated lactate levels increased global lactylation, with H4K12la as the predominant mark. H4K12la-targeted CUT&TAG analysis identified TRIM29 as a key regulator. H4K12la promotes TRIM29 transcription, which activates the PI3K-AKT pathway via direct and EGFR-mediated mechanisms, leading to autophagy inhibition and senescence. Interventions such as SIRT1 overexpression or intra-articular oxamate injection reduced lactylation, inhibited glycolysis, and mitigated cartilage degeneration. These findings demonstrate that glycolytic lactate-induced H4K12la fosters senescence through TRIM29-mediated PI3K-AKT activation, highlighting the inhibition of glycolysis or lactylation as a promising therapeutic strategy for OA. - Source: PubMed
Publication date: 2026/02/18
Zuo RongtaiWu ChenliangLin ZhiqiKong LingchiWang FengZhang XuanchengWei JianxingLin YiYang ErpengKang QinglinZhao ShichangGuan JunjieZhao Jinzhong - - Source: PubMed
Publication date: 2026/03/22
Hwang YoonjungHan Jae-HoHaam SeokjinLee Hyun WooKoh Young Wha