Ask about this productRelated genes to: DAZ2 antibody
- Gene:
- DAZ2 NIH gene
- Name:
- deleted in azoospermia 2
- Previous symbol:
- -
- Synonyms:
- pDP1678, MGC126442
- Chromosome:
- Yq11.223
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-25
- Date modifiied:
- 2015-08-27
Related products to: DAZ2 antibody
Related articles to: DAZ2 antibody
- Arabidopsis MYB transcription factor, AtDUO1 regulates generative cell body (GC) morphogenesis from round to semi and fully elongated forms before pollen mitosis-II (PM II). It was hypothesised that DUO1 might regulate morphogenesis through any of its direct target genes or components of the DUO1-DAZ1 network. The developmental analysis of plants harbouring T-DNA insertions in some DUO1 target genes using light and fluorescence microscopy revealed abnormal GC morphogenesis only in daz1 and daz2, but gcs1, trm16, mapkkk10, mapkkk20, tet11, and tip1 all undergo normal elongation indicating that these target genes have no important roles in morphogenesis or may be redundant. The important regulatory role of DUO1 was confirmed through the observed incomplete rescue of morphogenesis of mutant duo1-1 GCs by DAZ1 and independently by a C-terminally deleted version of DUO1 (DUO1∆C3) lacking activation sequences. The evidence supports the important role of DAZ1 in GC shape partial morphogenesis. The C-terminus of DUO1 may regulate some target genes that affect GC body elongation. Furthermore, an intact DUO1 is shown to be indispensable for GC shape and nucleus elongation and subsequently for timely division and sperm cell morphogenesis. The development of the GC cytoplasmic projection is regulated independently of DUO1, and all its target genes were able to form it. - Source: PubMed
Publication date: 2025/01/07
Rauf AbdurWang AnbangLi YujiaLian ZhihaoWei ShouxingKhan QayashJabbar KashmalaJan FarooqKhan IkramullahBibi MamoonaAbidullah SyedLi Jingyang - Advancements in sequencing technologies and assembly methods enable the regular production of high-quality genome assemblies characterizing complex regions. However, challenges remain in efficiently interpreting variation at various scales, from smaller tandem repeats to megabase rearrangements, across many human genomes. We present a PanGenome Research Tool Kit (PGR-TK) enabling analyses of complex pangenome structural and haplotype variation at multiple scales. We apply the graph decomposition methods in PGR-TK to the class II major histocompatibility complex demonstrating the importance of the human pangenome for analyzing complicated regions. Moreover, we investigate the Y-chromosome genes, DAZ1/DAZ2/DAZ3/DAZ4, of which structural variants have been linked to male infertility, and X-chromosome genes OPN1LW and OPN1MW linked to eye disorders. We further showcase PGR-TK across 395 complex repetitive medically important genes. This highlights the power of PGR-TK to resolve complex variation in regions of the genome that were previously too complex to analyze. - Source: PubMed
Publication date: 2023/06/26
Chin Chen-ShanBehera SairamKhalak AsifSedlazeck Fritz JSudmant Peter HWagner JustinZook Justin M - RAD51 is a critical recombinase that functions in concert with auxiliary mediator proteins to direct the homologous recombination (HR) DNA repair pathway. We show that Cys319 RAD51 possesses nucleophilic characteristics and is important for irradiation-induced RAD51 foci formation and resistance to inhibitors of poly (ADP-ribose) polymerase (PARP). We have previously identified that cysteine (Cys) oxidation of proteins can be important for activity and modulated via binding to peroxiredoxin 1 (PRDX1). PRDX1 reduces peroxides and coordinates the signaling actions of protein binding partners. Loss of PRDX1 inhibits irradiation-induced RAD51 foci formation and represses HR DNA repair. PRDX1-deficient human breast cancer cells and mouse embryonic fibroblasts display disrupted RAD51 foci formation and decreased HR, resulting in increased DNA damage and sensitization of cells to irradiation. Following irradiation cells deficient in PRDX1 had increased incorporation of the sulfenylation probe DAz-2 in RAD51 Cys319, a functionally-significant, thiol that PRDX1 is critical for maintaining in a reduced state. Molecular dynamics (MD) simulations of dT-DNA bound to a non-oxidized RAD51 protein showed tight binding throughout the simulation, while dT-DNA dissociated from an oxidized Cys319 RAD51 filament. These novel data establish RAD51 Cys319 as a functionally-significant site for the redox regulation of HR and cellular responses to IR. - Source: PubMed
Publication date: 2022/08/24
Skoko John JCao JuxiangGaboriau DavidAttar MyriamAsan AlparslanHong LisaPaulsen Candice EMa HongqiangLiu YangWu HanzhiHarkness TreyFurdui Cristina MManevich YefimMorrison Ciaran GBrown Erika TNormolle DanielSpies MariaSpies Michael AshleyCarroll KateNeumann Carola A - The precise contribution of each chromosome gene or gene family in achieving male fertility is still the subject of debate. Most studies have examined male populations with heterogeneous causes of infertility, and have therefore reached controversial or uncertain conclusions. This study uses Y-chromosome array-based comparative genomic hybridization (aCGH) to examine a population of males with a uniform sertoli cell-only syndrome (SCOS) infertility phenotype. - Source: PubMed
Publication date: 2022/03/28
Lan Kuo-ChungWang Hung-JenWang Tzu-JouLin Hsin-JungChang Yung-ChiaoKang Hong-Yo - The increase in intracellular calcium is influenced by cyclic nucleotides (cAMP and cGMP) content, which rating is governed by phosphodiesterases (PDEs) activity.Despite it has been demonstrated a beneficial effect of PDEs inhibitors in different pathological conditions involving SKM, not much is known on the role exerted by cAMP-cGMP/PDEs axis in human SKM contractility. Here, we show that Ssulfhydration of PDEs modulates human SKM contractility in physiological and pathological conditions. Having previously demonstrated that, in the rare human syndrome Malignant Hyperthermia (MH), there is an overproduction of hydrogen sulfide (HS) within SKM contributing to hyper-contractility, here we have used MH negative diagnosed biopsies (MHN) as healthy SKM, and MH susceptible diagnosed biopsies (MHS) as a pathological model of SKM hypercontractility. The study has been performed on MHS and MHN human biopsies after diagnosis has been made and on primary SKM cells derived from both MHN and MHS biopsies. Our data demonstrate that in normal conditions PDEs are S-sulfhydrated in both quadriceps' biopsies and primary SKM cells. This post translational modification (PTM) negatively regulates PDEs activity with consequent increase of both cAMP and cGMP levels. In hypercontractile biopsies, due to an excessive HS content, there is an enhanced Ssulfhydration of PDEs that further increases cyclic nucleotides levels contributing to SKM hyper-contractility. Thus, the identification of a new endogenous PTM modulating PDEs activity represents an advancement in SKM physiopathology understanding. - Source: PubMed
Publication date: 2022/02/01
Vellecco ValentinaPanza ElisabettaBibli Sofia-IrisCasillo Gian MarcoRaucci FedericaManzo Onorina LauraSmimmo MartinaVillani RomoloCavezza Maria RosariaFleming Ingridd'Emmanuele di Villa Bianca RobertaMaione FrancescoCirino GiuseppeBucci Mariarosaria