SUMO1 (recombinant) (aa 1_97)
- Known as:
- SUMO1 (Rec.) (aa 1_97)
- Catalog number:
- AR09173PU-L
- Product Quantity:
- 0.5 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SUMO1 (recombinant) ( 1_97)
Related genes to: SUMO1 (recombinant) (aa 1_97)
- Gene:
- AGAP11 NIH gene
- Name:
- ArfGAP with GTPase domain, ankyrin repeat and PH domain 11
- Previous symbol:
- -
- Synonyms:
- KIAA1975
- Chromosome:
- 10q23.2
- Locus Type:
- unknown
- Date approved:
- 2008-09-22
- Date modifiied:
- 2015-11-17
- Gene:
- ALG14 NIH gene
- Name:
- ALG14 UDP-N-acetylglucosaminyltransferase subunit
- Previous symbol:
- -
- Synonyms:
- MGC19780
- Chromosome:
- 1p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-08-09
- Date modifiied:
- 2019-01-18
- Gene:
- ANKHD1 NIH gene
- Name:
- ankyrin repeat and KH domain containing 1
- Previous symbol:
- -
- Synonyms:
- MASK, FLJ20288, FLJ11979, FLJ10042, FLJ14127, KIAA1085, MASK1
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-16
- Date modifiied:
- 2015-03-24
- Gene:
- ANKS3 NIH gene
- Name:
- ankyrin repeat and sterile alpha motif domain containing 3
- Previous symbol:
- -
- Synonyms:
- KIAA1977, FLJ32345, FLJ32767
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-17
- Date modifiied:
- 2014-11-19
- Gene:
- BUD23 NIH gene
- Name:
- BUD23 rRNA methyltransferase and ribosome maturation factor
- Previous symbol:
- WBSCR22
- Synonyms:
- MGC19709, MGC2022, MGC5140, PP3381, WBMT, MERM1
- Chromosome:
- 7q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-24
- Date modifiied:
- 2019-03-11
Related products to: SUMO1 (recombinant) (aa 1_97)
Related articles to: SUMO1 (recombinant) (aa 1_97)
- Cataract is a major cause of blindness among patients with diabetes mellitus. The pathology underlying diabetic cataract (DC) is complex because of changes in biological processes caused by chronic hyperglycemia. O-GlcNAcylation is highly dependent on glucose availability and regulates mitochondrial functions. Dysregulation of O-GlcNAcylation has been reported in DC. Mitochondria in lens epithelial cells are key organelles for energy supply and redox homeostasis of the lens. Mitochondrial dysfunction is a hallmark of DC. However, whether O-GlcNAcylation regulates mitochondrial function underlying DC has not been fully studied. - Source: PubMed
Guo ZaoxiaLi XinnanChen XiMa XiaopanYan Hong - Inhibited acute myeloid leukemia (AML) proliferation is accompanied by downregulated peroxisome proliferator-activated receptor α (PPARα), which however can be stabilized via SUMOylation. This study investigated how PPARα SUMOylation impacts AML cell growth. - Source: PubMed
Publication date: 2025/06/08
Song XiaoluShi FangfangWang XiaogangPeng YeWang HuafangJin LaiLan Jianping - Copper (Cu) and zinc (Zn) are essential trace metal elements for vertebrates, and insufficient intake of trace metal elements can have adverse effects on animal health. Studies suggested that the interaction among trace metal elements played a crucial role in this process. Therefore, the current study was conducted to explore whether low Zn alleviated low dietary Cu-induced decrease in intestinal Cu level and identify potential mechanisms via the in vivo animal experiment and in vitro cell culture. The regulatory relationship between metal response element binding transcription factor 1 (Mtf-1) and ATPase Cu transporting alpha (Atp7a) under low Cu and low Zn was elucidated through electrophoretic mobility shift assays and chromatin immunoprecipitation analysis. The SUMOylation modification of Mtf-1 and its effects on atp7a promoter were determined through immunoprecipitation and dual-luciferase reporter assay. Compared with the control, the low dietary Cu group significantly promoted the transcriptional regulation of atp7a promoter by Mtf-1, leading to intestinal Cu metabolism disorders. However, compared with the low dietary Cu group, the low Cu + low Zn group had significantly inhibited the transcriptional regulation of atp7a promoter by Mtf-1 and alleviated intestinal Cu metabolism disorder caused by low Cu. Mechanistically, Mtf-1 was modified by SUMOylation, and Sumo1-overexpression significantly reduced atp7a promoter activity. Taken together, dietary low Zn alleviated low Cu-induced decrease in intestinal Cu level through the SUMOylated-Mtf-1 and the Mtf-1/Atp7a axis. - Source: PubMed
Zhong Chong-ChaoYang HongHogstrand ChristerSong Chang-ChunZheng HuaHuang ChaoLuo Zhi - Myocardial ischemia-reperfusion injury (MIRI) exacerbates myocardial damage, resulting in a further decline in heart function. Abnormally high TRAF6 expression was reported in MIRI. However, what actually causes the abnormally elevated expression of TRAF6 in MIRI is still unclear and needs further study.Mice underwent left anterior descending (LAD) occlusion for 30 minutes and then reperfusion for 24 hours to establish our MIRI model. Hypoxia/reoxygenation (H/R) was used to treat AC16 cells. Morphology of myocardial tissues was examined by HE staining and myocardial infarction size was measured using Evans blue/TTC staining. The levels of vital molecules were determined using RT-qPCR, ELISA, and western blot. The interactions between molecules were validated by Co-IP. Cell viability and apoptosis were evaluated using CCK-8 and flow cytometry.Our results showed higher expressions of TRAF6 and SUMO1 in MIRI models. In addition, TRAF6 protein was modified by SUMOylation, thereby enhancing TRAF6 protein stability and TRAF6 expression. Of note, TIF1β mediated TRAF6 protein SUMOylation. Moreover, TRAF6 overexpression reversed TIF1β silencing-generated enhancement of cell viability and reductions in cell apoptosis and inflammatory response in H/R-induced AC16 cells.TIF1β mediated TRAF6 protein SUMOylation to stabilize TRAF6 protein and enhance TRAF6 level, thereby facilitating MIRI through inhibiting cell viability and enhancing cell apoptosis and inflammatory response. - Source: PubMed
Nan YueZhang XuDu XinpingZuo GuoxingLu Chengzhi - Atherosclerosis (AS)-associated cardiovascular disease is the main cause of global mortality. The excessive retention of glycated low-density lipoprotein (G-LDL) under the vascular endothelium promotes AS. In addition, G-LDL supports a role in promoting the expression of scavenger receptor A (SR-A), increasing SR-A-mediated transcytosis of G-LDL in endothelial cells (ECs), consequently accelerating the progression of atherosclerosis. However, the underlying mechanism used by G-LDL to promote SR-A expression has not been elucidated, thus representing the aim of this work. - Source: PubMed
Publication date: 2026/05/30
Shu MengCheng WenzhuoYu FangyangZhang LiyinWang LiShu YanWang RuonanXue BaoruiJin Si