ZNF445 antibody - middle region (ARP31987_P050)
- Known as:
- ZNF445 (anti-) - middle region (ARP31987_P050)
- Catalog number:
- arp31987_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF445 antibody - middle region (ARP31987_P050)
Related genes to: ZNF445 antibody - middle region (ARP31987_P050)
- Gene:
- ZNF445 NIH gene
- Name:
- zinc finger protein 445
- Previous symbol:
- ZNF168
- Synonyms:
- ZKSCAN15, ZSCAN47
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-02
- Date modifiied:
- 2016-10-05
Related products to: ZNF445 antibody - middle region (ARP31987_P050)
Related articles to: ZNF445 antibody - middle region (ARP31987_P050)
- Source: PubMed
- Multi-locus imprinting disturbance (MLID) with methylation defects in various differentially methylated regions (DMRs) has recently been identified in approximately 150 cases with imprinting disorders (IDs), and deleterious variants have been found in genes related to methylation maintenance of DMRs, such as those encoding proteins constructing the subcortical maternal complex (SCMC), in a small fraction of patients and/or their mothers. However, integrated methylation analysis for DMRs and sequence analysis for MLID-causative genes in MLID cases and their mothers have been performed only in a single study focusing on Beckwith-Wiedemann syndrome (BWS) and Silver-Russell syndrome (SRS) phenotypes. - Source: PubMed
Publication date: 2024/10/05
Urakawa TatsukiSoejima HidenobuYamoto KaoriHara-Isono KaoriNakamura AkieKawashima SayakaNarusawa HiromuneKosaki RikaNishimura YutakaYamazawa KazukiHattori TetsuoMuramatsu YukakoInoue TakanobuMatsubara KeikoFukami MakiSaitoh ShinjiOgata TsutomuKagami Masayo - Imprinting disorders are a group of congenital diseases which are characterized by molecular alterations affecting differentially methylated regions (DMRs). To date, at least twelve imprinting disorders have been defined with overlapping but variable clinical features including growth and metabolic disturbances, cognitive dysfunction, abdominal wall defects and asymmetry. In general, a single specific DMR is affected in an individual with a given imprinting disorder, but there are a growing number of reports on individuals with so-called multilocus imprinting disturbances (MLID), where aberrant imprinting marks (most commonly loss of methylation) occur at multiple DMRs. However, as the literature is fragmented, we reviewed the molecular and clinical data of 55 previously reported or newly identified MLID families with putative pathogenic variants in maternal effect genes (NLRP2, NLRP5, NLRP7, KHDC3L, OOEP, PADI6) and in other candidate genes (ZFP57, ARID4A, ZAR1, UHRF1, ZNF445). - Source: PubMed
Publication date: 2022/03/16
Eggermann ThomasYapici ElzemBliek JetPereda ArrateBegemann MatthiasRusso SilviaTannorella PierpaolaCalzari Lucianode Nanclares Guiomar PerezLombardi PaolaTemple I KarenMackay DeborahRiccio AndreaKagami MasayoOgata TsutomuLapunzina PabloMonk DavidMaher Eamonn RTümer Zeynep - ZNF445, as well as ZFP57, is involved in the postfertilization methylation maintenance of multiple imprinting-associated differentially methylated regions (iDMRs). Thus, ZNF445 pathogenic variants are predicted to cause multilocus imprinting disturbances (MLIDs), as do ZFP57 pathogenic variants. In particular, the MEG3/DLK1:IG-DMR would be affected, because the postzygotic methylation imprint of the MEG3/DLK1:IG-DMR is maintained primarily by ZNF445, whereas that of most iDMRs is preserved by both ZFP57 and ZNF445 or primarily by ZFP57. - Source: PubMed
Publication date: 2021/05/26
Kagami MasayoHara-Isono KaoriMatsubara KeikoNakabayashi KazuhikoNarumi SatoshiFukami MakiOhkubo YumikoSaitsu HirotomoTakada ShujiOgata Tsutomu - Genomic imprinting is an epigenetic process regulated by germline-derived DNA methylation that is resistant to embryonic reprogramming, resulting in parental origin-specific monoallelic gene expression. A subset of individuals affected by imprinting disorders (IDs) displays multi-locus imprinting disturbances (MLID), which may result from aberrant establishment of imprinted differentially methylated regions (DMRs) in gametes or their maintenance in early embryogenesis. Here we investigated the extent of MLID in a family harbouring a ZFP57 truncating variant and characterize the interactions between human ZFP57 and the KAP1 co-repressor complex. By ectopically targeting ZFP57 to reprogrammed loci in mouse embryos using a dCas9 approach, we confirm that ZFP57 recruitment is sufficient to protect oocyte-derived methylation from reprogramming. Expression profiling in human pre-implantation embryos and oocytes reveals that unlike in mice, ZFP57 is only expressed following embryonic-genome activation, implying that other KRAB-zinc finger proteins (KZNFs) recruit KAP1 prior to blastocyst formation. Furthermore, we uncover ZNF202 and ZNF445 as additional KZNFs likely to recruit KAP1 to imprinted loci during reprogramming in the absence of ZFP57. Together, these data confirm the perplexing link between KZFPs and imprint maintenance and highlight the differences between mouse and humans in this respect. - Source: PubMed
Monteagudo-Sánchez AnaHernandez Mora Jose RamonSimon CarlosBurton AdamTenorio JairLapunzina PabloClark StephenEsteller ManelKelsey GavinLópez-Siguero Juan Pedrode Nanclares Guiomar PerezTorres-Padilla Maria-ElenaMonk David