ZNF285A Blocking Peptide
- Known as:
- ZNF285A Blocking Peptide
- Catalog number:
- 33r-7442
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- ZNF285A Blocking Peptide
Related genes to: ZNF285A Blocking Peptide
- Gene:
- ZNF285 NIH gene
- Name:
- zinc finger protein 285
- Previous symbol:
- ZNF285A
- Synonyms:
- -
- Chromosome:
- 19q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-17
- Date modifiied:
- 2016-11-09
Related products to: ZNF285A Blocking Peptide
Related articles to: ZNF285A Blocking Peptide
- Non-alcoholic fatty liver disease (NAFLD), recently retermed as metabolic dysfunction-associated steatotic liver disease (MASLD), and intervertebral disc degeneration (IVDD) are major health burdens with rising prevalence. Despite affecting different organ systems, emerging evidence suggests potential molecular crosstalk between these conditions. However, the underlying mechanisms remain poorly understood. - Source: PubMed
Publication date: 2026/01/26
Wang GuohaoLiu YongmingShen Xingchao - Hepatocellular carcinoma (HCC) is one of the most prevalent and aggressive forms of liver cancer, with high morbidity and poor prognosis due to late diagnosis and limited treatment options. Despite advances in understanding its molecular mechanisms, effective biomarkers for early detection and targeted therapy remain scarce. Zinc finger protein 71 (ZNF71), a zinc-finger protein, has been implicated in various cancers, yet its role in HCC remains largely unexplored. This gap in knowledge underscores the need for further investigation into the ZNF71 of potential as a diagnostic or therapeutic target in HCC. - Source: PubMed
Qin KaiXiong Dan-DanQin ZhenLi Ming-JieLi QiHuang Zhi-GuangTang Yu-XingLi Jian-DiZhan Yan-TingHe Rong-QuanLuo JieWang Hai-QuanZhang Shu-QiChen GangWei Dan-MingDang Yi-Wu - Secretory breast carcinoma (SBC) is one of the rarest breast carcinomas and currently lacks a standard treatment regimen. To date, few reports on double primary SBCs have been published, especially regarding the tumors' genomic features. A 51-year-old woman with early SBC who developed a secondary SBC in the contralateral mammary tissue 140 months later was evaluated. Here, we describe for the first time the sequencing results of a Chinese patient with nonsimultaneous double-primary SBC. In addition to the ETV6-NTRK3 fusion, variants in polymorphisms of enzymes related to drug metabolism variant genes, including BCL2L11, CYP2B6, CYP2C19, ERCC1, GSTM1, GSTP1, MTHFR, NQO1, TYMS, and XRCC, were present according to 425-gene DNA sequencing. The ETV6-NTRK3 fusion site was different between the tumors; furthermore, whole-gene exon sequencing revealed that genetic variation spectrum of the two tumors was different. A POLDIP2 mutation was found in the first tumor, and HDLBP, MMP2, PLEKHA6 and ZNF285 variants were detected in the second tumor. Our findings further our understanding of the molecular pathogenesis of SBCs, especially regarding tumors occurring at different times in one patient. Further molecular analyses of such cases are warranted to improve targeted therapies for SBC. - Source: PubMed
Publication date: 2022/07/01
Lei TingDeng XuPeng YanChen Tongbing - Although recent genome-wide association studies have identified risk loci that strongly associates with autism spectrum disorder (ASD), how to pinpoint the causal genes remains a challenge. We aimed to pinpoint the potential causal genes and explore the possible susceptibility and mechanism. A convergent functional genomics (CFG) method was used to prioritize the candidate genes by combining lines of evidence, including Sherlock analysis, spatio-temporal expression patterns, expression analysis, protein-protein interactions, co-expression and association with brain structure. A higher score in the CFG approach suggested that more evidence supported this gene as an ASD risk gene. We screened genes with higher CFG scores for candidate functional single nucleotide polymorphisms (SNPs). A genotyping experiment (602 ASD children and 604 healthy sex-matched children) and the dual-luciferase reporter gene assay were followed to validate the effects of SNPs. We identified three genes (MAPT, ZNF285, and TIGD5) as candidate causal genes using the CFG approach. The genotyping experiment showed that TIGD5 rs75547282 was associated with an increased risk of ASD under the dominant model (OR = 1.37, 95% CI = 1.09-1.72, P = 0.006) though the statistical power was limited (5.2%). The T allele of rs75547282 activated the expression of TIGD5 compared with the C allele in the dual-luciferase reporter assay. Our study indicates that such comprehensive integrative analyses may be an effective way to explore promising ASD susceptibility variants and needs to be further investigated in future research. Genotyping experiments should, however, be based on a larger population sample to increase statistical power. LAY SUMMARY: We set out to pinpoint the potential causal genes of ASD and explore the possible susceptibility and mechanism by combining lines of evidence from different analyses. Our results show that TIGD5 rs75547282 is associated with the risk of ASD in the Han Chinese population. In addition, a similar framework to seek promising ASD risk variants could be further investigated in future research Autism Res 2021, 14: 631-644. © 2021 International Society for Autism Research and Wiley Periodicals LLC. - Source: PubMed
Publication date: 2021/01/04
Xie XinyanLi LiWu HaoHou FangChen YanlinXue QiZhou YuZhang JiajiaGong JianhuaSong Ranran