SOX21 monoclonal antibody (M02), clone 3H4
- Known as:
- SOX21 mab (anti-) (M02), clonality 3H4
- Catalog number:
- H00011166-M02
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- SOX21 monoclonal antibody (M02) clone 3H4
Related genes to: SOX21 monoclonal antibody (M02), clone 3H4
- Gene:
- EMC10 NIH gene
- Name:
- ER membrane protein complex subunit 10
- Previous symbol:
- C19orf63
- Synonyms:
- INM02, HSS1, HSM1
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2007-07-17
- Date modifiied:
- 2016-12-01
- Gene:
- MRPL1 NIH gene
- Name:
- mitochondrial ribosomal protein L1
- Previous symbol:
- -
- Synonyms:
- BM022
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-28
- Date modifiied:
- 2015-08-25
- Gene:
- PMS2 NIH gene
- Name:
- PMS1 homolog 2, mismatch repair system component
- Previous symbol:
- PMSL2
- Synonyms:
- H_DJ0042M02.9, HNPCC4, MLH4
- Chromosome:
- 7p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-13
- Date modifiied:
- 2019-04-23
- Gene:
- SESN2 NIH gene
- Name:
- sestrin 2
- Previous symbol:
- -
- Synonyms:
- SES2, DKFZp761M0212, HI95, SEST2
- Chromosome:
- 1p35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-03
- Date modifiied:
- 2016-10-05
- Gene:
- SOX21 NIH gene
- Name:
- SRY-box 21
- Previous symbol:
- -
- Synonyms:
- SOX25
- Chromosome:
- 13q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-14
- Date modifiied:
- 2015-11-23
Related products to: SOX21 monoclonal antibody (M02), clone 3H4
Related articles to: SOX21 monoclonal antibody (M02), clone 3H4
- Tooth morphogenesis is controlled by various molecules, and the enamel knot plays a important role as a signaling center. Here, we aimed to analyze the role of AmeloD in the development of the enamel knot. - Source: PubMed
Publication date: 2026/02/12
Oka SaeChiba YutaSato HiroshiChiba MistukiKomine ItaruHirofuji YutaYamada AyaFukumoto Satoshi - The first lineage decision in mammalian development segregates embryonic and extra-embryonic fates, yet the timing of this specification remains under debate. While our previous lineage tracing studies in mice and human suggested that this decision is initiated as early as the 2-cell stage, prevailing models place its onset to the 16-cell stage embryo when the first inside cells form. In mice, we have found that heterogeneous expression of Sox21 at the 4-cell stage contributes to fate specification, with higher SOX21 levels biasing cells toward embryonic fates (future foetus). Here, we investigated whether this heterogeneity originates even earlier. Because conventional single-cell RNA-seq has failed to detect mRNA asymmetries prior to the 4-cell stage, we employed a more sensitive approach, confocal imaging combined with hybridization chain reaction (HCR), to track Sox21 mRNA expression from the zygote through the 4-cell stage. This single-molecule technique revealed pronounced heterogeneity in Sox21 transcript levels as early as the 2-cell stage. Intriguingly, Sox21 mRNA appears to be preferentially expressed from the male pronucleus during minor zygotic genome activation, perhaps as a consequence of H3K27me3 enrichment in the maternal pronuclei and given that haploid parthenogenetic embryos lack SOX21 protein at the 4-cell stage. These findings provide evidence that Sox21 mRNA heterogeneity arises earlier than previously recognized, namely at the 2-cell stage. Our work supports the emerging view that spatial mRNA distribution, long appreciated in non-mammalian embryos, might also contribute to lineage specification in mammals. - Source: PubMed
Publication date: 2026/02/13
Sanchez-Vasquez EstefaniaNawarungruang GydaMeglicki MaciejBronner Marianne EZernicka-Goetz Magdalena - Treatment-resistant glioblastoma stem and precursor cells (GPCs) drive glioblastoma (GBM) growth and recurrence. Thus, targeting the molecular machinery that sustains GPCs in an undifferentiated and self-renewing state is a promising therapeutic strategy. The transcription factor SOX21 effectively suppresses the tumorigenic capacity of GPCs, but the mechanism by which SOX21 impedes GPC features is unknown. By engineering patient-derived GPCs with a transgenic TetOn system we show that SOX21 expression induces an anti-tumorigenic transcriptional program, aligning with clinical data demonstrating a positive correlation between SOX21 levels and improved GBM patient survival. Induced SOX21 expression in GPCs within pre-established GBM reduces their capacity to sustain tumor growth and significantly extends the survival of the orthotopically transplanted mice. Mechanistically, SOX21 functions as a tumor suppressor by binding a large set of AP-1-targeted chromatin regions, leading to epigenetic repression of AP-1-activated genes. Consistently, the anti-tumorigenic activities of SOX21 are largely replicated by AP-1 inhibitors, which decrease GPC proliferation and survival, while overexpression of the AP-1 family member, c-JUN, counteracts these effects. Our findings identify SOX21 as a key regulator that prevents GPC malignancy by targeting and repressing an AP-1-driven, tumor-promoting gene expression program. These results highlight SOX21-regulated pathways as promising therapeutic targets for GBM. - Source: PubMed
Publication date: 2026/01/31
Rrapaj EltjonaYuan JuanKurtsdotter IdhaMisyurin VsevolodBaselli Guido AlessandroHolmberg JohanPersson OscarBergsland MariaMuhr Jonas - This study reports differential expression of Antisense RNAs (asRNAs) by analyzing transcriptomic profiles in gallbladder cancer (GBC). - Source: PubMed
Rajput MonikaDixit RuhiPandey ManojShukla Vijay Kumar - Morphologic sex differences between males and females typically emerge after the primordial germ cell migration and gonad formation, although sex is determined at fertilization based on chromosome composition. A key debated sexual difference is the embryonic developmental rate, with in vitro produced male embryos often developing faster. However, the molecular mechanisms driving early embryonic sex differences remain unclear. - Source: PubMed
Publication date: 2025/08/27
Shi MeihongLi GuangshengAraujo Hannah MarieLee Angie SZhang JingzhiLee Yoke Lee Cheong Soon HonDuan Jingyue Ellie