WAPL antibody Polyclonal Antibodies Primary antibodies
- Known as:
- WAPL (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100628
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- WAPL antibody Polyclonal Antibodies Primary antibodies
Related genes to: WAPL antibody Polyclonal Antibodies Primary antibodies
- Gene:
- WAPL NIH gene
- Name:
- WAPL cohesin release factor
- Previous symbol:
- KIAA0261, WAPAL
- Synonyms:
- FOE
- Chromosome:
- 10q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-21
- Date modifiied:
- 2016-10-05
Related products to: WAPL antibody Polyclonal Antibodies Primary antibodies
Related articles to: WAPL antibody Polyclonal Antibodies Primary antibodies
- Cervical cancer remains a major global health challenge despite advances in human papillomavirus (HPV) vaccination, screening, and treatment. Persistent infection with high-risk HPV types, particularly HPV16 and HPV18, is a necessary cause of cervical cancer; however, only a small fraction of infections progress to malignancy, indicating the importance of additional cofactors. Increasing evidence identifies estrogen signaling as a critical modifier of HPV-driven carcinogenesis. Estrogen acts synergistically with HPV oncogenes E6 and E7 to promote genomic instability, immune evasion, and tumor progression, largely through effects on the tumor microenvironment (TME). This review aims to clarify and summarize current knowledge on the interplay between HPV biology, estrogen signaling, and the cervical cancer microenvironment, discussing HPV structure, life cycle, and mechanisms of oncogenesis including viral genome integration, disruption of tumor suppressor pathways, and induction of chromosomal instability. Particular emphasis is placed on estrogen receptor signaling, highlighting the shift from tumor cell-intrinsic estrogen receptor α (ERα) expression to a paracrine, stromal-driven mechanism during disease progression. Estrogen signaling in cancer-associated fibroblasts, myeloid-derived suppressor cells, and regulatory T cells fosters an immunosuppressive microenvironment that supports viral persistence and malignant transformation. Both classical genomic and rapid non-genomic estrogen pathways are discussed, as well as their roles in immune modulation and DNA damage responses. Furthermore, there is emerging evidence linking estrogen signaling to HPV-induced genomic instability through pathways involving G protein-coupled estrogen receptor 1 (GPER1), estrogen receptor α36 (ERα36), High Mobility Group AT-Hook 2 (HMGA2), and wings apart-like (WAPL). Finally, the review contextualizes these molecular insights within contemporary clinical management, summarizing standard treatments and recent advances in targeted and immunotherapies, including bevacizumab and pembrolizumab. Understanding estrogen-driven stromal-immune crosstalk in HPV-associated cervical carcinogenesis may uncover novel therapeutic opportunities. Integrating hormonal modulation with immunotherapy and other targeted strategies represents a promising avenue to improve outcomes, particularly in advanced and treatment-resistant disease. - Source: PubMed
Publication date: 2026/05/21
Kao Pei-YuChen Jie-HongChen Kuo-Hu - Quantitative interpretation of ChIP-seq data is instrumental to derive insight into chromatin and transcription factor biology. Here we developed ChIP-FRiP, an end-to-end pipeline enabling systematic comparison of pairwise protein positioning, and applied it to the study of cohesin. In mammalian interphase, loop extruding cohesin complexes are positioned by CTCF barriers to generate locus-specific 3D genome folding patterns. Many aspects of our understanding of cohesin loop extrusion come from interpreting the amount of cohesin ChIP-seq signal at CTCF barriers, which has been reported to change variably after perturbing cohesin co-factors, such as NIPBL, PDS5A/B, and WAPL. Using ChIP-FRiP to homogeneously process 140 cohesin ChIP-seq datasets from 13 publicly available studies, we observed substantial variation attributable to technical effects, obscuring biological interpretability. To better understand how technical considerations, such as antibody specificity, influence apparent cohesin binding patterns, we integrated technical aspects of ChIP-seq into biophysical simulations of loop extrusion. Leveraging a simple biochemical model for background ChIP-seq signal, we derived a strategy to estimate and correct for the background using paired spike-in ChIP-seq data from wild-type and depletion conditions. Our results establish a framework for reliable comparative analysis, demonstrating that accurate background correction is requisite for interpreting the roles of cohesin cofactors in cohesin positioning. - Source: PubMed
Publication date: 2026/02/27
Xiao YaoAnderson Erika CRahmaninejad HadiNora ElphègeFudenberg Geoffrey - Cohesin-NIPBL complexes extrude genomic DNA into loops that are constrained by CTCF boundaries. This process has important regulatory functions and weakens the separation between euchromatic and heterochromatic compartments. Cohesin can also bind PDS5 proteins, which do not support loop extrusion but are required for the formation of CTCF boundaries. How PDS5 proteins perform this function is unknown. Here we show, by in vitro single-molecule imaging, that human PDS5 proteins stop loop extrusion by facilitating the dissociation of NIPBL from cohesin. Hi-C experiments suggest that this function is required for the establishment of CTCF boundaries in cells. In silico modeling indicates that PDS5 proteins enable the separation between compartments by limiting cohesin's velocity and chromatin residence time. The degree of this compartmentalization depends on the frequency with which chromatin is extruded relative to the time it takes for compartments to form. These results identify PDS5 proteins as key regulators of genome organization. - Source: PubMed
Publication date: 2026/04/23
Wutz GordanaDavidson Iain FBanigan Edward JStocsits Roman RKawasumi RyotaroTang WenNagasaka KotaCostantino LorenzoJansen RalfHirota KoujiBranzei DanaMirny Leonid APeters Jan-Michael - expression is regulated by a distal enhancer cluster known as the control region (SCR). Although and the SCR exhibit strong interactions in chromosome conformation capture experiments, acute depletion of cohesin only mildly affects transcription. Here we show that continuous restarting of loop extrusion, but not stalling of cohesin at CTCF sites, is involved in the maintenance of the -SCR loop. While depletion of cohesin or CTCF has only a mild impact on gene expression, stabilizing cohesin on the DNA by depleting the cohesin release factor WAPL results in a rapid decrease in expression. Furthermore, using genome editing, we show that a weak enhancer located downstream from the gene renders expression insensitive to the loss of cohesin stalling at CTCF sites. Finally, through targeted and pleiotropic inhibition of the SCR, we demonstrate that the -SCR loop is a multicomponent system that depends on cohesin-mediated loop extrusion and enhancer-associated factors. Together, our findings highlight the intricate interplay between enhancer activity and loop extrusion in the establishment and maintenance of chromatin loops in the locus. - Source: PubMed
Publication date: 2026/06/01
Martinovic MorenoFlach Koen Dde Kort Marit A CMaresca MichelaTeunissen HansLiu Ning QingLenstra Tineke Lde Wit Elzo - Cohesin is a fundamental genome-organizing complex that orchestrates three-dimensional chromosome folding and gene expression via DNA loop extrusion. Alterations to genes encoding cohesin subunits and cohesin loaders cause Mendelian disorders, including Cornelia de Lange syndrome (CdLS). By contrast, disruption of factors that remove cohesin from DNA, including and its binding partners and , have not yet been associated with human disease. Here, we explored the relevance of these cohesin release factors in Mendelian disease by establishing a rare disease cohort of deeply phenotyped individuals with heterozygous, predicted damaging variants in (n=27), (n=8), and (n=8), by modeling deficiency in human cell lines and mice, and by aggregating rare disease association statistics from consortia studies. We identified a -related disorder characterized by developmental delay, intellectual disability, and risk of other developmental anomalies including clubfoot. Similarities between individuals with damaging variants and those with large, recurrent 10q22.3q23.2 (10q) deletions (which encompass ) nominate as a driver gene within this genomic disorder region. While carriers of or variants exhibited features of developmental disorders, neither cohort-based statistics nor case phenotyping associated these genes with specific phenotypes. We used CRISPR engineering to generate truncating variants in , as well the 7.8 Mb 10q deletion or duplication in human iPSCs and induced neurons. Transcriptomic analyses identified differentially expressed genes in both models, with highly significant overlap between haploinsufficiency and 10q deletion signatures. Mice with 50% residual expression exhibited mild deficits of growth and learning/memory, whereas those with 25% residual expression displayed birth defects and postnatal lethality, revealing a dosage liability threshold below the level of heterozygosity. In summary, we delineated a novel genetic condition caused by cohesin release factor deficiency, nominated as a driver gene within a genomic disorder region, and further illuminated dosage sensitivity of human cohesin. - Source: PubMed
Publication date: 2026/02/28
Boone Philip MErdin SerkanMohamed AbucarHaghshenas SadeghehFaour Kamli N WKao EmelineFu JackAuwerx ChiaraHarripaul RicardoJana BimalSpringer DanielleHallstrom Greyde Esch Celine E FDenhoff EricaHolmes LaurenMohajeri KianaLemanski JohnKerkhof JenniferMcConkey HaleyRzasa JessicaMcCune Madison JLevy Michael AGrafstein JuliaLarson MatthewWright ZsabreBeauchamp Roberta LLucente DianeJamra Rami AbouAgrawal NeenaAgrawal PankajAndersen Erica FArgilli EmanuelaAraiza ReneeBallal SoniaBaxter Megan FBergant GaberBertsche AstridBhavsar RiyaBortola Debora RBothe ViktoriaBrasch-Andersen CharlotteBraun DominiqueBruel Ange-LineBuchanan CatherineBurt Nicholas DCarvalho Laura M LChiriatti LuigiCogne BenjaminCollins RyanCrunk AmyCurrall BenjaminDelahaye-Duriez AndreeDelanne JulianDenommé-Pichon Anne-SophieDevriendt KoenraadDomingo AloysiusDuncan LauraFaivre LaurenceFamularo LauraFulton AnneGenetti CasieHarel TamarHavlovicova MarketaHiggs JennyHoulier MarineIascone MariaImmken LaDonnaIsidor BertrandKaiser Frank JKarbone KayceeKenna MargaretKhan AmjadKimmig Lara KristinaKleefstra TjitskeKraus Eva-MariaKrepischi Ana C VKrey IlonaLadda RogerLanoue LouiseLe Caignec CedricLewis Zoe KLima GloriaLynch Sally AnnMacek MilanMaier OlivierMaitz SilviaMale AlisonMalikova MarcelaMcKay VictoriaMoldovan OanaMonteil DanielleOliveira Mariana MoysésMunasinghe JeevaNakamori SachikoNeuser SonjaNizon MathildeNuttle XanderO'Keefe KathrynOrec LauraParenti IlariaPeterlin BorutPfundt RolphPouncey JillRadio Francesca ClementinaRobert LeemaRodan LanceRosenberg-Fogler HallelRosenfeld Jill ASafraou HanaSalani MonicaSchliesske SophiaSeaby Eleanor GSell SusanEliot Shearer ASherr ElliottShillington AmelleSiebold DorotheaSinnema MargjeSmith LauraStegmann Alexander P AStevens CathyStevens ServiSurette EricTartaglia MarcoTaylor Jenny CThompson Michelle LTørring Pernille MMau Them Frederic TranTsoulaki OlgaUmair MuhammadVanhoutte ElsVincent MarieVitobello Antoniovon Wintzingerode LydiaWatt AmyWayhelova MarketaWentzensen Ingrid MWilson WilliamWojcik Monica HYuan BoZampino GiuseppeSrivastava SiddharthWestphal Dominik SRiedhammer Korbinian MJoyce EricYadav RachitaGusella JamesTai Derek J CSadikovic BekimPfeifer Karl ETalkowski Michael E