GATA6 EMSA Kit
- Known as:
- GATA6 EMSA Kit
- Catalog number:
- AY1098
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- GATA6 EMSA Kit
Related genes to: GATA6 EMSA Kit
- Gene:
- GATA6 NIH gene
- Name:
- GATA binding protein 6
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 18q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-11
- Date modifiied:
- 2016-10-05
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- Embryonic development demands precise coordination of transcriptional and post-transcriptional mechanisms to ensure rapid cell fate transitions, yet the molecular mechanisms by which RNA influences these transitions remain unclear. Here, we observed a global increase in mRNA stability during the blastocyst formation, which precedes rapid lineage specification. Using both in vivo and mouse totipotent blastomere-like cells (TBLCs) or extended pluripotent stem cells (EPSCs) differentiation systems, we demonstrate that this transcriptome-wide stabilization is essential for the second cell fate decision, particularly in the formation of primitive endoderm (PrE). Mechanistically, VIRMA and METTL3, the components of methyltransferase complex (MTC) establish lineage specification by stabilizing the key PrE transcription factors, including Gata6, via the N-methyladenosine (mA) reader IGF2BP3. Knocked down of these regulatory proteins or targeted removal of mA on Gata6, impacted the differentiation of PrE both in vivo and in vitro, and caused defects in blastulation and blastoid formation. Our results demonstrate that mA-dependent post-transcriptional regulation plays a pivotal role in shaping lineage specification during peri-implantation and provided potential strategies for rescuing developmental defects. - Source: PubMed
Publication date: 2026/04/28
Xiao WeideTang LiMa MingliLiu KuishengLu JiaxuDing WenqingBai ZhileLiu XuelianKou XiaochenZhao YanhongWang HongYang LeiGao ShaorongGao YaweiLiu Jun - Endometrial receptivity lacks robust biomarkers. Given its role in stabilizing the progesterone receptor, the epigenetic regulator BMI1 is a key candidate, yet its clinical potential is undefined. This study aimed to characterize BMI1's expression and functional role in receptivity and evaluate its utility as a biomarker for predicting reproductive outcomes. - Source: PubMed
Publication date: 2026/04/08
Liu MeiliMao JianaYao YanyanTu LiliZhang Kemei - Mutations in BMP4 have been associated with malformations of the urinary tract in human patients. Genetic studies in mice have shown that these defects are linked to the expression of Bmp4 in the mesenchymal primordium of the ureter, where it acts as a critical signal for coordinated cytodifferentiation of the mesenchymal and epithelial tissues. Here, we used unbiased transcriptional profiling of ureters with genetic depletion of Bmp4 and pharmacological inhibition of BMP4 signaling to decipher the gene regulatory network controlled by BMP4 in the early ureter, focusing on transcription factors as possible drivers of cytodifferentiation. We show that in Bmp4-deficient ureters, expression of Grhl3, Msx2, Pparg, Trp63 and Foxa1 in the epithelial compartment, and of Gata6, Hopx, Id2, Id4, Myocd, Snai1 and Tbx18 in the mesenchymal primordium is reduced. Expression of Msx2, Pparg, Gata6, Id genes, Tbx18 and Snai1 requires direct BMP4 signaling input, whereas reduced expression of the other genes is likely due to secondary changes, including increased retinoic acid signaling. Conditional gene targeting of Smad4 revealed that BMP4-dependent activation of transcription factor genes is mediated in part by SMAD effectors in both ureteral tissues. Thus, our work links BMP4 (signaling) to known transcriptional regulators of ureteral cytodifferentiation and uncovers additional factors that may be relevant to this program. - Source: PubMed
Publication date: 2026/04/22
Deuper LenaHense NicolasBeckers AnjaThiesler HaukeMamo Tamrat MBergmann FlorianHildebrandt HerbertTrowe Mark-OliverKispert Andreas - Therapeutic mesenchymal stromal cells (MSCs) promote healing in severe injuries like skin burns. However, expansion on stiff culture surfaces activates MSCs into scar-promoting myofibroblasts. We previously introduced 'mechanical memory' to describe how MSCs primed on scar-stiff surfaces retain myofibroblast traits even after switching to softer, skin-like surfaces. Now, we identify mechanisms and factors that suppress myofibroblast activation during priming in soft cultures. These 'soft memory' factors are poised to preserve MSC regenerative features while preventing fibrogenesis. Mechanically primed MSCs were compared via RNA- and ATAC-sequencing to co-analyze gene transcription and chromatin accessibility. Highly accessible promoters of genes upregulated after soft priming, which retained this pattern after transitioning to stiff surfaces, were enriched for HOXA11 transcription factor binding motifs. Knocking down HOXA11 increased osteogenic gene expression in soft-primed MSCs and reduced anti-fibrotic factors, including the transcription factor SALL1, which suppresses pro-fibrotic genes like Postn, Col8a1, Grem2, Thbs1, Thbs2, and Gata6. We identify GATA6 as a keeper of stiff-induced myofibroblast memory after switching to soft surfaces. Manipulating the SALL1-GATA6 circuit yielded therapeutic MSCs that suppressed fibrosis in a hypertrophic skin-scarring animal model. Therefore, controlling myofibroblast memory could improve MSC-based organ repair therapies. - Source: PubMed
Publication date: 2026/04/22
Younesi Fereshteh SadatMiller Andrew EDiao LiGuo XinyingAndonian NatalieKarimizadeh ElhamBarker Thomas HHinz Boris - Distal bile duct carcinoma (DBDC) and pancreatic ductal adenocarcinoma (PDAC) are aggressive malignancies; however, their metachronous occurrence within a short postoperative timeframe is extremely rare. We present an extremely rare case of diffuse-type PDAC that rapidly developed only 16 months after curative resection of DBDC. - Source: PubMed
Publication date: 2026/04/17
Tomioka AtsushiKawaguchi NaoKurisu YoshitakaUeda YasuhikoKushiyama ShuheiHamamoto HirokiTanaka RyoImai YoshiroKomeda KojiAsakuma MitsuhiroTomiyama HidekiLee Sang-Woong