ZFP95 antibody - N-terminal region (ARP31830_T100)
- Known as:
- ZFP95 (anti-) - N-terminal region (ARP31830_T100)
- Catalog number:
- arp31830_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZFP95 antibody - N-terminal region (ARP31830_T100)
Related genes to: ZFP95 antibody - N-terminal region (ARP31830_T100)
- Gene:
- ZKSCAN5 NIH gene
- Name:
- zinc finger with KRAB and SCAN domains 5
- Previous symbol:
- ZFP95
- Synonyms:
- ZNF914, ZSCAN37
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-23
- Date modifiied:
- 2016-10-05
Related products to: ZFP95 antibody - N-terminal region (ARP31830_T100)
Related articles to: ZFP95 antibody - N-terminal region (ARP31830_T100)
- Hepatocellular carcinoma (HCC), the most prevalent form of liver cancer, has a high incidence and mortality rate. This study aimed to elucidate the function of MEX3A in HCC and explore its underlying mechanisms. The expression of MEX3A was assessed in a DEN/CCl-induced mouse model and in clinical HCC tumor tissues. MEX3A expression was increased in the tumors of HCC patients and was associated with poor prognosis. CRISPR/Cas9-mediated MEX3A knockout induced cell cycle arrest at the G0/G1 phase and suppressed the proliferation of HCC cells. Knockout of Mex3a hampered tumor development in DEN/CCl-induced mice and inhibited xenograft tumor growth. MEX3A reduces the mRNA stability of DHRS3 via MRE. Knockdown of DHRS3 compromised the effect of MEX3A knockout on the HCC cell cycle and promoted HCC development. MEX3A transcription in HCC is regulated by ZKSCAN5. Knockout of ZKSCAN5 induced HCC cell cycle arrest at the G0/G1 phase and suppressed HCC cell proliferation. Sincalide, a compound targeting ZKSCAN5, inhibited the malignant behavior of HCC cells. The findings of this study indicate that sincalide serves as a potential ZKSCAN5-targeting candidate compound. By binding to ZKSCAN5 and promoting its proteasome-dependent degradation, it offers a new avenue for inhibiting the ZKSCAN5/MEX3A/DHRS3 axis. - Source: PubMed
Publication date: 2026/09/09
Li WeihanMo ShanshanZhang WeiBen YiranChen Guolin - The aim of the work was to identify the features of associations of single nucleotide polymorphisms (SNPs) that determine the level of sex hormones in the body with simple endometrial hyperplasia without atypia (EnH) in women with different body mass index (BMI). Two groups of BMI-differing subjects (BMI < 25 [n = 766]: 196 EnH, 570 control and BMI ≥ 25 [n = 727]: 324 EnH, 403 control) with a total number of 1493 women were formed to conduct this study. Nine SNPs meaningful for the level of sex hormones (proven in genome-wide association studies [GWAS]) such as rs34670419 [G>T] , rs148982377 [T>C] , rs11031002 [T>A] , rs11031005 [T>C] , rs112295236 [C>G] , rs117145500 [A>C] , rs727428 [C>T] , rs1641549 [C>T] , rs117585797 [C>A] were considered by us. In general, in the studied sample (EnH/control, n = 1493), an association of interactions of rs148982377 [T>C] × BMI with EnH (OR = 1.11) was revealed. As a result of a comparative analysis, we found that rs148982377 [T>C] was associated with EnH in women with a BMI ≥ 25 (OR = 1.77) and was not linked with the disease in women with a BMI < 25. Both common protective factors for EnH were also identified in women with BMI ≥ 25 and BMI < 25 (rs11031002 [T>A] (OR = 0.43 and OR = 0.46 respectively) and rs11031005 [T>C] (OR = 0.46 and OR = 0.58 respectively)). At the same time, in the BMI ≥ 25 cohort, the risk effect of the TT*rs11031002-rs11031005 haplotype (OR = 3.27) was more pronounced, and the contribution of interlocus interactions of sex hormone genes with EnH formation was more significant (7 SNPs in 12 models) than in the BMI < 25 group (OR = 2.31 and 4 SNPs in 3 models). In conclusion, the presented work is exploratory and demonstrates differences in the nature of the association with EnH in women with different BMI of the testosterone-determining polymorphism: SNP rs148982377 [T>C] was associated with EnH in women with a BMI ≥ 25 and was not linked with the disease in women with a BMI < 25. - Source: PubMed
Publication date: 2026/06/02
Churnosov VladimirChurnosova MariaReshetnikov EvgenyAristova InnaTsoy KirillSorokina InnaPolonikov AlexeySolodilova MariaChurnosov MikhailPonomarenko Irina - Prostate cancer is a great substantial health challenge among the cancer type with a high incidence and serving as the main cause of cancer-related deaths in men. Apolipoprotein C1 encodes a member of the apolipoprotein C family. The APOC1 has been confirmed as an oncogene of prostate cancer. However, the mechanism of how the APOC1 protein influence remains to be elucidated. - Source: PubMed
Publication date: 2025/09/30
Liu YongboQi ZihaoYang ShuoLi YanzeGuo Jia - Lysosomal-associated transmembrane protein 5 (LAPTM5) has been associated with poor prognosis in cancer patients. Its role in regulating metastasis in pancreatic ductal adenocarcinoma (PDAC), however, remains vague. The study here aimed to expound the metastasis-promoting properties of LAPTM5 in PDAC and the detailed mechanism. LAPTM5 was overexpressed in metastatic PDAC cells and was related to the dismal prognosis of patients in GEO datasets. By using lentiviral vectors harboring short hairpin RNA, we found that LAPTM5 downregulation reduced PDAC cell viability, proliferation, and aggressiveness and liver metastasis . Zinc finger with KRAB and SCAN domains 5 (ZKSCAN5) was predicted and verified to mediate LAPTM5 transcription in PDAC cells. Both ZKSCAN5 and SET domains, containing lysine methyltransferase 7 (SETD7) bound to the LAPTM5 promoter, and ZKSCAN5 recruited SETD7 to form a complex promoting LAPTM5 transcription. LAPTM5 knockdown reversed the promoting effect of ZKSCAN5 on the metastasis of PDAC cells. Thus, our findings on the ZKSCAN5/SETD7/LAPTM5 axis provide insights into the underlying mechanism of liver metastasis dissemination in PDAC. - Source: PubMed
Publication date: 2023/11/22
Yang YongXie WeiQiao XuanYang JunYao DanZhu Dongming - The most important driver gene in malignant melanoma is the BRAF mutation, and molecularly targeted therapies targeting mutations, mainly V600E and V600k, are used in clinical practice. In this report, we treated a patient with malignant melanoma expressing a rare BRAF-ZKSCAN5 fusion gene with dabrafenib/trametinib. The patient was a 71-year-old female. She was diagnosed with malignant melanoma (pT4aN3M0, STAGE IIIC) of the abdomen with axillary lymph node metastasis. She underwent extended resection and axillary lymph node dissection and was treated with adjuvant therapy, but lung and mediastinal lymph node metastases developed. The patient was treated with immune checkpoint inhibitors for metastatic lesions and achieved complete remission, but relapsed and metastatic lesions appeared in the cervical lymph nodes. Next-generation sequencing revealed the BRAF-ZKSCAN5 fusion gene, and treatment with dabrafenib/trametinib was initiated. After 1 month of treatment, tumor growth stopped and the length of the tumor shrank by 22.2%, but she developed grade 3 adverse events of nausea, fatigue, and diarrhea and had difficulty exercising, forcing her to discontinue treatment after 6 weeks. The tumor continued to shrink during drug administration. This case report may provide insight into treatment options for cases in which the BRAF fusion gene was observed, which is expected to be detected in large numbers by next-generation sequencing in the future. - Source: PubMed
Publication date: 2023/09/22
Kato HiroshiKano ShinjiYasui YukikoNojiri YukaYoshimitsu MakiNakamura MotokiMorita Akimichi