GATA2 (Phospho-Ser401) Antibody
- Known as:
- GATA2 (Phospho-Ser401) Antibody
- Catalog number:
- 11691
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- GATA2 (Phospho-Ser401) Antibody
Related genes to: GATA2 (Phospho-Ser401) Antibody
- 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 (Phospho-Ser401) Antibody
Related articles to: GATA2 (Phospho-Ser401) Antibody
- 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 - Aplastic anemia (AA) is a disease characterized by a severe reduction of the erythroid lineage. Its molecular mechanisms have been studied using technologies such as whole-exome sequencing via NGS; however, this remains a costly and limited-access strategy for developing countries. In this study, 17 de novo patients diagnosed with AA were analyzed. Genomic DNA was isolated from each patient to perform the Multiplex Ligation-dependent Probe Amplification (MLPA) technique, which uses different probes to detect numerical alterations in the exons of the genes of interest (GATA2, RUNX1, C/EBPα, hTERT). In 70.9% cases, a molecular abnormality was found. GATA2 was the most frequently altered gene (58.8%), followed by TERT (47.0%), RUNX1 (41.1%), and finally C/EBPα (35.3%). Detecting these molecular alterations could help to understand the progression of AA to other hematologic malignancies due to the genomic instability associated with this panel of genes involved in various hematopoietic maturation processes. - Source: PubMed
Publication date: 2026/05/15
Salas Iveth MendozaCarrillo Irma OlarteMaldonado Rafael CerónLaguna Anel Iraís GarcíaRosas Adrián De la CruzPeñafiel Christian Omar RamosFigueroa Efreen Horacio MontañoRocha Diana Laura CarrilloMurillo Carlos MartínezBarroso Verónica Fabiola MoránTovar Adolfo Martínez - Mechanical forces altered after unilateral pneumonectomy (PNX) control post-PNX lung growth. Here, we demonstrate that post-PNX endothelial regeneration is stimulated at the peripheral region of the mouse lung, requiring the focal adhesion (FA) protein, paxillin, while inhibition of mechanical tension attenuates the effects. Paxillin mediates stretching-induced YAP1-TEAD1 signaling, which stimulates GATA2 activity on angiogenic factor angiopoietin-2 (ANGPT2) transcription in endothelial cells (ECs), dictating post-PNX endothelial regeneration at the peripheral region. Deleting endothelial paxillin suppresses expression of GATA2 in the specific EC subtype, capillary type 1 ECs (CAP1s) following PNX. Extracellular matrix protein, collagen VI that impacts cell mechanical responses is expressed more at the peripheral region in the post-PNX mouse lungs, which drives paxillin expression, leading to EC regeneration. Mechanosensitive paxillin signaling in ECs mediates spatial control of post-PNX endothelial regeneration. - Source: PubMed
Publication date: 2026/05/18
Mammoto TadanoriKyi PriscillaScheer MikaelaHunyenyiwa TendaiHashemi ElahehMa XiaolongTurner Christopher ELin Chien-WeiMalarkannan SubramaniamMammoto Akiko