GATA2 antibody - N-terminal region (ARP31855_T100)
- Known as:
- GATA2 (anti-) - N-terminal region (ARP31855_T100)
- Catalog number:
- arp31855_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GATA2 antibody - N-terminal region (ARP31855_T100)
Related genes to: GATA2 antibody - N-terminal region (ARP31855_T100)
- Gene:
- GATA2 NIH gene
- Name:
- GATA binding protein 2
- Previous symbol:
- -
- Synonyms:
- NFE1B
- Chromosome:
- 3q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-03
- Date modifiied:
- 2019-04-23
Related products to: GATA2 antibody - N-terminal region (ARP31855_T100)
Related articles to: GATA2 antibody - N-terminal region (ARP31855_T100)
- GATA2 deficiency predisposes patients to recurrent infections, myelodysplastic neoplasms (MDSs), and malignancies through disrupted hematopoiesis and immune dysfunction. The role of the gut microbiome (GM) in this condition remains poorly defined. In this multicenter study, we analyzed GM composition, metabolomic, and lipidomic profiles in 12 Italian GATA2-deficient patients, comparing non-HSCT and post-HSCT GATA2-deficient individuals with healthy controls. Non-HSCT patients showed a relative enrichment of Proteobacteria-associated Gram-negative taxa, accompanied by increased levels of metabolites and lipids previously associated with inflammatory processes. Post-HSCT patients displayed profiles with a trend toward partial normalization of GM composition and metabolic features. Overall, our findings suggest the presence of microbiome and metabolic patterns in GATA2-deficient patients, which may reflect underlying immune and hematopoietic alterations, although these observations should be interpreted as descriptive and require validation in larger cohorts. - Source: PubMed
Publication date: 2026/05/12
Roncareggi SamueleFioredda FrancescaGirardi KatiaSerrao SimoneCapitoli GiuliaFumagalli RebeccaNobile MartaFazio GraziaGuerra FabiolaValsecchi Maria GraziaRebellato StefanoCasillo MarikaFantuz Maria RosariaSavarese GiovanniPaglia GiuseppeGambineri EleonoraBalduzzi Adriana CristinaBiondi AndreaSaettini Francesco - Adipogenesis is governed by a complex interplay between transcriptional regulation and epigenetic remodeling. While many transcriptional pathways have been well characterized, less is known about how chromatin-level regulation shapes the timing of gene expression, particularly in large animal models such as pigs. In this study, we investigated histone modification patterns associated with four key adipogenic transcription factor genes-, , , and -in porcine mesenchymal stem cells (MSCs) undergoing adipogenic differentiation. - Source: PubMed
Publication date: 2026/04/28
Aksoy Mehmet OnurWozniak JakubStachowiak MonikaSzczerbal Izabela - High-altitude hypoxia (HAH) can cause adverse reactions, such as tinnitus and barotrauma, but the role of mitotic catastrophe (MC) in HAH remains unreported. This study investigated MC-associated biomarkers in HAH. - Source: PubMed
Publication date: 2026/05/21
Zhao WenwenLiu DefangLuo TingWu Yang - Polycystic ovary syndrome (PCOS) is a common endocrine disorder that contributes to pregnancy complications like Intra Uterine Growth Restriction (IUGR), leading to compromised foetal outcome. Although maternal metabolic and hormonal imbalances are well-established in PCOS, the specific molecular alterations within the placenta and its outcome remains poorly explored. This study aimed to characterize key molecular signaling alterations in PCOS placentae with respect to steroid hormone receptors, trophoblast lineage specification, along with their structural alterations. To understand the above alterations, PCOS rodent mothers were developed using letrozole treatment for 21days daily orally, following which induction of pregnancy and those pregnant animals were sacrificed at GD18. Tissues were subjected to expression levels of steroidal and placental cell markers using transcriptomic and protein expression, along with morphometric and histological analysis, correlated with hormone profile. Histological analysis of GD 18 PCOS placenta exhibited a reduction in labyrinth zone, with an increased AR expression, along with downregulation of PR, ER ɑ and ER β, indicating an altered steroidal status. Moreover, dysregulation of genes such as Phlda2, Tpbpa, Pcdh12, Prl3b1, CDX2, GCM1, and GATA2 along with reduced expression of SynA, Syn B were observed suggesting an impaired trophoblast differentiation, vascular development, and immune tolerance. Additionally, elevated expressions of Flt4, H2K and IFN gamma suggested compensatory mechanisms attempting to offset placental dysfunction. This study clearly indicates maternal PCOS pathophysiology effects placental development by altering the morphology, along with abnormal hormonal homeostasis, contributing to impaired differentiation. These findings underscore the importance of targeting placental pathways in the management of PCOS-related pregnancy outcomes. - Source: PubMed
Publication date: 2026/05/21
Mahapatra AnanyaPillai GautamiRana RemiShah ZeelNampoothiri Laxmipriya - Hematopoietic stem cell (HSC) transplantation is an established therapy for malignant and nonmalignant hematologic disorders; however, clinical application remains constrained by limited graft availability and challenges in maintaining stemness during ex vivo manipulation, as well as transplant-related complications. Accordingly, alternative strategies to generate hematopoietic-competent cells from accessible stem cell sources are being actively explored. This study investigated whether overexpression enhances the hematopoietic trans-differentiation potential of dental tissue-derived mesenchymal stem cells (DMSCs) and whether the resulting HSC-like cells exert therapeutic effects in a cyclophosphamide-induced myelosuppressed mouse model following intra-femoral delivery. was introduced into DMSCs using the Neon transfection system, and -overexpressing DMSCs (DMSCs) were subsequently exposed to hematopoietic cytokines to induce an HSC-like phenotype. Cytokine-treated DMSCs exhibited a rounded morphology, increased expression of HSC-associated surface markers (CD34 and CD45), and upregulated hematopoietic transcription factors, including , , , and . The derived HSC-like cells (D-HSCs) were transplanted into the femoral bone marrow cavity of myelosuppressed mice, and therapeutic outcomes were assessed by complete blood counts and histological analyses. D-HSC transplantation was associated with recovery of bone marrow cellularity and partial restoration of spleen and thymus cellularity and size, accompanied by improvement in body weight and peripheral blood parameters compared with myelosuppressed controls. Collectively, these findings indicate that -enhanced DMSCs can be directed toward an HSC-like state under hematopoietic cues and that the resulting cells may support hematopoietic and immune recovery in myelosuppressed hosts, supporting their potential as an alternative, autologous cell source for hematopoietic regeneration. - Source: PubMed
Publication date: 2026/05/20
Han Jang-HoLee Sang-YunJo Chan-HeeSon Young-BumLee Won-JaeLee Hyeon-JeongHong Chae-YeonPark SanghyeonKang Seo-YoonHwang Tae-SungKim JaeminLee Sung-LimChoe Yong-HoRho Gyu-Jin