MYST4 Blocking Peptide
- Known as:
- MYST4 Blocking Peptide
- Catalog number:
- 33r-6590
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- MYST4 Blocking Peptide
Related genes to: MYST4 Blocking Peptide
- Gene:
- KAT6B NIH gene
- Name:
- lysine acetyltransferase 6B
- Previous symbol:
- MYST4
- Synonyms:
- querkopf, qkf, Morf, MOZ2, ZC2HC6B
- Chromosome:
- 10q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-03
- Date modifiied:
- 2016-02-12
Related products to: MYST4 Blocking Peptide
Related articles to: MYST4 Blocking Peptide
- We report a case of a uterine mesenchymal tumor with myogenic differentiation and SRF::RELA fusion occurring in a 23-year-old woman manifesting as an endometrial polyp. The tumor consisted of bland spindle cells with a predominantly fascicular growth pattern and entrapment of the endometrial glands and vessels. The tumor was positive for smooth muscle markers and CD10. NGS RNA analysis revealed SRF::RELA fusion. NGS DNA analysis revealed no pathogenic variants or copy-number alterations. On follow-up 12 months after curettage, the patient showed no signs of the disease. To the best of our knowledge, only 3 cases of uterine tumors with SRF::RELA fusion arising in the gynecologic tract have been described previously, and all show benign behavior so far. Differential diagnosis includes both benign and potentially aggressive entities, such as leiomyoma, inflammatory myofibroblastic tumor, perivascular epithelioid cell tumor, uterine adenosarcoma, low-grade endometrial stromal sarcoma, and uterine sarcoma with KAT6B/A::KANSL1 fusion. - Source: PubMed
Publication date: 2026/08/05
Manethová MonikaHojný JanDundr Pavel - uterine sarcoma has been recently recognized as a distinct type of uterine sarcoma displaying mixed endometrial stromal and smooth muscle features. - Source: PubMed
Publication date: 2026/07/13
Chen LaurenLiu JiahuiNechala IsabellePraveen Kumar PoojaEwanowich CarolLevecchia MelissaAubrey ChristaFu YangxinLee Cheng-Han - Coarctation of the aorta (CoA) is a congenital narrowing of the aortic isthmus near the ductus arteriosus or ligamentum arteriosum. Despite successful anatomical repair, patients remain at risk of recoarctation, arterial hypertension, and diffuse aortopathy, suggesting intrinsic vessel-wall abnormalities beyond localized obstruction. The developmental and molecular basis of these persistent vascular features remains incompletely understood. Human aortic tissue samples were obtained from 8 male infants with CoA and 6 age- and sex-matched controls aged <1 year. Total RNA was isolated, and gene expression profiling was performed using whole human genome oligo microarrays (Agilent). Differentially expressed transcripts were subjected to pathway, network, and upstream regulator analyses using Ingenuity Pathway Analysis (IPA, Qiagen). Selected candidate genes were evaluated by RT-qPCR in independent verification sets. Transcriptomic profiling identified 402 analysis-ready transcripts distinguishing CoA from control tissue. Exploratory pathway analyses suggested extracellular matrix remodeling characterized by collagen turnover, integrin-mediated cell-matrix interactions, wound-healing signaling, and fibrosis-associated programs. In addition, enrichment analyses identified developmental annotations involving retinoic acid (RA)/RAR/RXR signaling, -associated developmental programs, and a shared -associated signature. Network and upstream regulator analyses further suggested associations with cytoskeletal, muscle-associated, and epigenetic regulatory pathways, including , , retinoic acid/RAR/RXR signaling, , , and RT-qPCR independently confirmed increased expression of , , , and Infantile CoA tissue exhibited molecular signatures consistent with vessel-wall remodeling accompanied by developmental, vascular signaling, and smooth muscle/cytoskeletal regulatory programs. These findings support the hypothesis that developmental patterning signals and postnatal extracellular matrix remodeling coexist within CoA tissue and may contribute to persistent vascular abnormalities beyond anatomical repair. Given the exploratory nature of the study, these observations should be considered hypothesis-generating and require validation in independent cohorts. - Source: PubMed
Publication date: 2026/07/03
Robl Isabell GCesnjevar RobertEkici Arif BUebe SteffenJohann Pascal DRamirez Maria Daniela HernandezFincke Victoria EFahlbusch Fabian BMoosmann Julia - Uterine mesenchymal tumours represent a group of heterogeneous tumours, the classification of which is evolving, especially in the context of a broader use of molecular testing. Some entities can be diagnosed based on the combination of morphological and immunohistochemical features. In other entities, such as endometrial sarcomas with KAT6B/A::KANSL1 fusion, the correct diagnosis cannot currently be achieved without molecular testing. In this review, we focus on some of the new entities in which molecular testing plays an essential role for diagnosis, including tumours with KAT6B/A::KANSL1 fusion, tumours with MEIS1::NCOA2 fusion, and tumours with fusion involving the KDM2B gene. In addition, uterine tumours with whorling and GREB1:CTNNB1 fusion and endometrial stromal tumours with CTNNB1 mutation will be discussed. Other tumours with recurrent molecular alterations not specific to a single entity (such as tumours with PLAG1 fusion or RAD51B fusion) are also mentioned. In summary, molecular testing is a very important part of the classification of uterine mesenchymal tumours. The growing number of emerging entities helps to correctly classify tumours into clinically significant categories. However, these entities should be viewed with caution until their clinical significance is supported by robust data, and molecular findings should always be correlated with morphological features. - Source: PubMed
Dundr PavelKendall Bártů MichaelaHojný JanMatěj RadoslavNěmejcová Kristýna - Several studies have demonstrated the value of large-scale human exome and genome data analysis to maximise gene discovery in rare diseases. Using this approach, we have analysed the exomes of 4747 cases and 52,881 controls to identify genes which confer a substantial risk of congenital heart disease (CHD). We identified both rare loss-of-function and missense coding variants in 14 genes, which reached genome-wide significance at FDR 5%. Ten genes have been associated with CHD, whereas four genes (PBX1, KAT6B, SHOX2, HCAR1) have not been reported as genome-wide significant so far. We highlight distinct genetic contributions to syndromic and non-syndromic CHD by independently analysing probands from these two groups. In addition, by integrative analysis of exome data with single-cell transcriptomics data from human embryonic hearts, we identified cardiac-specific cells, such as neural crest cells and endothelial cells, as well as putative biological processes underlying the pathogenesis of CHD. In summary, our findings strengthen the association of known CHD genes and have identified additional novel disease genes contributing to the aetiology of CHD. - Source: PubMed
Publication date: 2026/06/02
Audain EnriqueWilsdon AnnaDombrowsky GregorSifrim AlejandroBreckpot JeroenPerez-Riverol YassetLoughna SiobhanDaly AllanAntoniou PavlosHofmann PhilippPerez-Riverol AmilcarKahlert Anne-KarinBauer UlrikePickardt ThomasKlaassen SabineBerger FelixDaehnert IngoDittrich SvenStiller BrigitteAbdul-Khaliq HashimBu'lock FrancesUebing AnselmKramer Hans-HeinerIyer VivekLarsen Lars AllanBrook J DavidHitz Marc-Phillip