C1orf77{Homo sapiens DKFZP547E1010 protein}rabbit.pAb
- Known as:
- C1orf77{Homo sapiens DKFZP547E1010 protein}host: rabbit.pAb
- Catalog number:
- 201-20-0727
- Product Quantity:
- 0.1ml
- Category:
- -
- Supplier:
- Shanghai Sunred
- Gene target:
- C1orf77{Homo sapiens DKFZP547E1010 protein}rabbit.pAb
Related genes to: C1orf77{Homo sapiens DKFZP547E1010 protein}rabbit.pAb
- Gene:
- CHTOP NIH gene
- Name:
- chromatin target of PRMT1
- Previous symbol:
- C1orf77
- Synonyms:
- DKFZP547E1010, SRAG, FOP
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-20
- Date modifiied:
- 2017-07-11
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- Chemotherapy resistance remains a significant challenge in colorectal cancer (CRC) treatment, with disrupted redox balance playing a central role. Here we identify CHTOP as a key regulator of oxidative stress and chemoresistance in CRC. Mechanistically, CHTOP promotes NRF2 transcriptional activity by recruiting the SENP3-containing 5FMC complex to deSUMOylate NRF2, thereby sustaining HO-1 expression and redox balance. Notably, CHTOP expression itself is tightly controlled by a feedback mechanism. The p52 isoform of PSIP1 inhibits CHTOP expression by interfering with HNRNPH1-mediated splicing, leading to CHTOP degradation via nonsense-mediated decay (NMD). Conversely, elevated oxidative stress stabilizes SENP3, which promotes deSUMOylation and degradation of p52, thereby relieving p52-mediated suppression of CHTOP expression. This establishes an oxidative stress-SENP3-p52-CHTOP feedback loop that fine-tunes CHTOP levels. In 5-FU-resistant CRC cells, CHTOP downregulation shifts cells into an elevated oxidative stress state, which correlates with reduced 5-FU sensitivity. Notably, either restoring CHTOP expression or further depleting CHTOP disrupts this redox balance and resensitizes resistant cells to 5-FU. These findings suggest that modulating CHTOP expression may offer a therapeutic strategy to overcome chemoresistance in CRC through redox regulation. - Source: PubMed
Publication date: 2026/08/15
Li JingLi XiaopengZhao ChenyeWu PeiwenHu WeibinZhao XuMa YuanDong ZepengYuan HangChen ShihuiChen ZiluLu JingWang WeiSun XuejunZhang QinMu Mingchao - This study focused on the intricate connections between hypertension nephropathy (HN) and diabetic nephropathy (DN) in terms of molecular and pathological mechanisms. The samples were from the Gene Expression Omnibus (GEO) database. GSE37460 and GSE142153 are training sets, and GSE37455 and GSE30529 are validation sets. We found 42 shared differentially expressed genes (DEGs) by means of the differential analysis. The GO/KEGG and GSEA analysis mainly highlights the signal transduction pathways related to the proteasome and cytokines. The eight hub genes identified through the Protein-Protein Interaction (PPI) network analysis include NR4A1, TNFSF10, CX3CR1, EGF, THBD, CXCR4, CCL5, and ATF3. Single-cell sequencing analysis revealed that TNFSF10 and NR4A1 were the most highly expressed in the cells of both HN and DN. Furthermore, five significant microRNAs identified include hsa-miR-1248, hsa-miR-200b-5p, hsa-miR-23b-5p, hsa-miR-3059-5p, and hsa-miR-3065-3p. Six essential transcription factors (TFs) (NFIL3, STAT3, NFKB1, USF1, USF2, and EGR1), 11 important drug chemicals (Cisplatin, Cyclosporine, perfluorooctanoic acid, Quercetin, Tretinoin, bisphenol A, Curcumin, Valproic Acid, Particulate Matter, Simvastatin, and Cadmium), seven related diseases (Atherosclerosis, Glioblastoma, Pulmonary Fibrosis, Asthma, Hepatitis B, Hepatitis C, and Diabetes Mellitus), and ten important RNA-binding proteins (RBPs) (CHTOP, EIF4E, HNRNPK, IGF2BP3, YTHDF3, HNRNPA2B1, RBM47, YBX1, RBFOX2, and RBM10). Finally, molecular docking simulations suggest that Tretinoin and Curcumin may have potential therapeutic value for both HN and DN. This study provides novel therapeutic targets for the combined diagnosis and treatment of HN and DN. - Source: PubMed
Publication date: 2025/06/03
Wang YanminWang YimingJin JingMa Bing - Somatic variants in the cancer genome influence gene expression through diverse mechanisms depending on their specific locations. However, a systematic evaluation of the effects of somatic variants located in 3' untranslated regions (3' UTRs) on alternative polyadenylation (APA) of mRNA remains lacking. In this study, we analyze 10,199 tumor samples across 32 cancer types and identify 1333 somatic single nucleotide variants (SNVs) associated with abnormal 3' UTR APA. Mechanistically, these 3' UTR SNVs can alter cis-regulatory elements, such as the poly(A) signal and UGUA motif, leading to changes in APA. Minigene assays confirm that 3' UTR SNVs in multiple genes, including RPS23 and CHTOP, induce aberrant APA. Among affected genes, 62 exhibit differential stability between tandem 3' UTR isoforms, including HSPA4 and UCK2, validated by experimental assays. Finally, we establish that SNV-related abnormal APA usage serves as an additional layer of expression regulation for tumor-suppressor gene HMGN2 in breast cancer. Collectively, this study reveals 3' UTR APA as a critical mechanism mediating the functional impact of somatic noncoding variants in human cancers. - Source: PubMed
Publication date: 2025/03/17
Xu QiushiCheng XiaomengLi QianruYu PengZhou XiaolanChen YuLin LiminNi TingZhao Zhaozhao - Superoxide Dismutase 3 (SOD3) scavenges extracellular superoxide giving a hydrogen peroxide metabolite. Both Reactive Oxygen Species diffuse through aquaporins causing oxidative stress and biomolecular damage. SOD3 is differentially expressed in cancer and this research utilises Gene Expression Omnibus data series GSE2109 with 2,158 cancer samples. Genome-wide expression correlation analysis was conducted with SOD3 as the seed gene. Categorical SOD3 Pearson Correlation gene lists incrementing in correlation strength by 0.01 from ρ≥|0.34| to ρ≥|0.41| were extracted from the data. Positively and negatively SOD3 correlated genes were separated for each list and checked for significance against disease overlapping genes in the ClinVar and Orphanet databases via Enrichr. Disease causal genes were added to the relevant gene list and checked against Gene Ontology, Phenotype Ontology, and Elsevier Pathways via Enrichr before the significant ontologies containing causal and non-overlapping genes were reviewed with a literature search for possible disease and oxidative stress associations. 12 significant individually discriminated disorders were identified: Autosomal Dominant Cutis Laxa (p = 6.05x10-7), Renal Tubular Dysgenesis of Genetic Origin (p = 6.05x10-7), Lethal Arteriopathy Syndrome due to Fibulin-4 Deficiency (p = 6.54x10-9), EMILIN-1-related Connective Tissue Disease (p = 6.54x10-9), Holt-Oram Syndrome (p = 7.72x10-10), Multisystemic Smooth Muscle Dysfunction Syndrome (p = 9.95x10-15), Distal Hereditary Motor Neuropathy type 2 (p = 4.48x10-7), Congenital Glaucoma (p = 5.24x210-9), Megacystis-Microcolon-Intestinal Hypoperistalsis Syndrome (p = 3.77x10-16), Classical-like Ehlers-Danlos Syndrome type 1 (p = 3.77x10-16), Retinoblastoma (p = 1.9x10-8), and Lynch Syndrome (p = 5.04x10-9). 35 novel (21 unique) genes across 12 disorders were identified: ADNP, AOC3, CDC42EP2, CHTOP, CNN1, DES, FOXF1, FXR1, HLTF, KCNMB1, MTF2, MYH11, PLN, PNPLA2, REST, SGCA, SORBS1, SYNPO2, TAGLN, WAPL, and ZMYM4. These genes are proffered as potential biomarkers or therapeutic targets for the corresponding rare diseases discussed. - Source: PubMed
Publication date: 2024/10/31
Stanworth MarkZhang Shu-Dong - Stratifying patient risk and exploring the tumor microenvironment are critical endeavors in prostate cancer research, essential for advancing our understanding and management of this disease. - Source: PubMed
Publication date: 2024/05/06
Zhou ShanSun LiMao FeiChen Jing