ZNF764 Over-expression Lysate Product
- Known as:
- ZNF764 Over-expression Lysate Product
- Catalog number:
- GWB-DA604E
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- ZNF764 Over-expression Lysate Product
Related genes to: ZNF764 Over-expression Lysate Product
- Gene:
- ZNF764 NIH gene
- Name:
- zinc finger protein 764
- Previous symbol:
- -
- Synonyms:
- MGC13138
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-14
- Date modifiied:
- 2015-01-12
Related products to: ZNF764 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: ZNF764 Over-expression Lysate Product
- Asthenozoospermia, a type of male infertility, is primarily caused by dysfunctional sperm mitochondria. Despite previous bioinformatics analysis identifying potential key lncRNAs, miRNAs, hub genes, and pathways associated with asthenospermia, there is still a need to explore additional molecular mechanisms and potential biomarkers for this condition. - Source: PubMed
Publication date: 2024/05/28
Lu HuiZhao LiqiangWang AnguoRuan HailingChen XiaoyanLi YejuanHu JiajiaLu WeiyingXiao Meifang - The C2H2-type zinc finger protein ZNF764 acts as an enhancer for several steroid hormone receptors, and haploinsufficiency of this gene may be responsible for tissue resistance to multiple steroid hormones including glucocorticoids observed in a patient with 16p11.2 microdeletion. We examined genome-wide regulatory actions of ZNF764 on the glucocorticoid receptor (GR) in HeLa cells as a model system. ZNF764- and GR-binding sites demonstrated similar distribution in various genomic features. They positioned predominantly around 50-500 kbs from the transcription start sites of their nearby genes, and were closely localized with each other, overlapping in ~37% of them. ZNF764 demonstrated differential on/off effects on GR-binding and subsequent mRNA expression: some genes were highly dependent on the presence/absence of ZNF764, but others were not. Pathway analysis revealed that these 3 gene groups were involved in distinct cellular activities. ZNF764 physically interacted with GR at ligand-binding domain through its KRAB domain, and both its physical interaction to GR and zinc finger domain appear to be required for ZNF764 to regulate GR transcriptional activity. Thus, ZNF764 is a cofactor directing GR transcriptional activity toward specific biologic pathways by changing GR binding and transcriptional activity on the glucocorticoid-responsive genes. - Source: PubMed
Publication date: 2017/01/31
Fadda AbeerSyed NajeebMackeh RafahPapadopoulou AnnaSuzuki ShigeruJithesh Puthen VKino Tomoshige - Nuclear hormone receptors exert their transcriptional effects through shared cofactor molecules; thus, defects in such intermediate proteins may be associated with multiple hormone resistance. Microdeletion of small chromosomal segments results in hereditary or sporadic diseases by affecting expression of residing genes. - Source: PubMed
Publication date: 2012/05/10
Kino TomoshigePavlatou Maria GMoraitis Andreas GNemery Robin LRaygada MargaritaStratakis Constantine A