| Transcription factor Nkx2-3 maintains the self-renewal of hematopoietic stem cells by regulating mitophagy. | Transcription factor Nkx2-3 maintains the self-renewal of hematopoietic stem cells by regulating mitophagy.
Hu M, Chen N, Chen M, Chen F, Lu Y, Xu Y, Yang L, Zeng H, Shen M, Chen X, Chen S, Wang F, Wang S, Wang J. | 06/13/2023 |
| Ameliorated Autoimmune Arthritis and Impaired B Cell Receptor-Mediated Ca(2+) Influx in Nkx2-3 Knock-out Mice. | Ameliorated Autoimmune Arthritis and Impaired B Cell Receptor-Mediated Ca(2+) Influx in Nkx2-3 Knock-out Mice.
Khanfar E, Olasz K, Gábris F, Gajdócsi E, Botz B, Kiss T, Kugyelka R, Berki T, Balogh P, Boldizsár F., Free PMC Article | 02/27/2021 |
| the inactivation of Nkx2-3 permits postnatal seeding, and its blocking effect on SILT maturation prevails at later stage. | Differential Effects of the Absence of Nkx2-3 and MAdCAM-1 on the Distribution of Intestinal Type 3 Innate Lymphoid Cells and Postnatal SILT Formation in Mice.
Vojkovics D, Kellermayer Z, Gábris F, Schippers A, Wagner N, Berta G, Farkas K, Balogh P., Free PMC Article | 07/18/2020 |
| These results hint at a previously unknown stromal role of Nkx2.3 as driver of colitis and indicate that Nkx2.3(+) stromal cells play a role in epithelial cell homeostasis. | IL-22-Independent Protection from Colitis in the Absence of Nkx2.3 Transcription Factor in Mice.
Kellermayer Z, Vojkovics D, Dakah TA, Bodó K, Botz B, Helyes Z, Berta G, Kajtár B, Schippers A, Wagner N, Scotto L, O'Connor OA, Arnold HH, Balogh P. | 01/11/2020 |
| results indicate that EDA/NKX2-3 signaling is essential for enamel knot formation during tooth morphogenesis in mice | The transcription factor NKX2-3 mediates p21 expression and ectodysplasin-A signaling in the enamel knot for cusp formation in tooth development.
Han X, Yoshizaki K, Miyazaki K, Arai C, Funada K, Yuta T, Tian T, Chiba Y, Saito K, Iwamoto T, Yamada A, Takahashi I, Fukumoto S., Free PMC Article | 04/6/2019 |
| Studies suggest oncogenic NK2 homeobox 3 homeobox protein (NKX2-3) in lymphomagenesis, and show a mouse model for studying the biology and therapy of human marginal-zone B-cell lymphomas. | Homeobox NKX2-3 promotes marginal-zone lymphomagenesis by activating B-cell receptor signalling and shaping lymphocyte dynamics.
Robles EF, Mena-Varas M, Barrio L, Merino-Cortes SV, Balogh P, Du MQ, Akasaka T, Parker A, Roa S, Panizo C, Martin-Guerrero I, Siebert R, Segura V, Agirre X, Macri-Pellizeri L, Aldaz B, Vilas-Zornoza A, Zhang S, Moody S, Calasanz MJ, Tousseyn T, Broccardo C, Brousset P, Campos-Sanchez E, Cobaleda C, Sanchez-Garcia I, Fernandez-Luna JL, Garcia-Muñoz R, Pena E, Bellosillo B, Salar A, Baptista MJ, Hernandez-Rivas JM, Gonzalez M, Terol MJ, Climent J, Ferrandez A, Sagaert X, Melnick AM, Prosper F, Oscier DG, Carrasco YR, Dyer MJ, Martinez-Climent JA., Free PMC Article | 10/6/2018 |
| Nkx2-3 deficiency reprograms the endothelial addressin preference for lymphocyte homing in Peyer's patches. | Absence of Nkx2-3 homeodomain transcription factor reprograms the endothelial addressin preference for lymphocyte homing in Peyer's patches.
Kellermayer Z, Mihalj M, Lábadi Á, Czömpöly T, Lee M, O'Hara E, Butcher EC, Berta G, Balogh A, Arnold HH, Balogh P. | 02/28/2015 |
| the organ-specific patterning of splenic vasculature is critically regulated by Nkx2-3, thereby profoundly affecting the lymphocyte homing mechanism and blood filtering capacity of the spleen in a tissue-specific manner. | Transcription factor Nkx2-3 controls the vascular identity and lymphocyte homing in the spleen.
Czömpöly T, Lábadi A, Kellermayer Z, Olasz K, Arnold HH, Balogh P. | 10/8/2011 |
| The splenic vascular defects in Nkx2-3 deficiency include the generation of LYVE-1(+) cysts, comprised of endothelial cells without being committed along the LEC lineage. | Absence of Nkx2-3 homeodomain transcription factor induces the formation of LYVE-1-positive endothelial cysts without lymphatic commitment in the spleen.
Kellermayer Z, Lábadi A, Czömpöly T, Arnold HH, Balogh P., Free PMC Article | 08/20/2011 |
| Formation of various white pulp fibroblast subsets is differentially affected by the presence of Nkx2.3 activity, possibly also influencing their role in various immune functions linked with complement activation and deposition. | Complex organizational defects of fibroblast architecture in the mouse spleen with Nkx2.3 homeodomain deficiency.
Bovári J, Czömpöly T, Olasz K, Arnold HH, Balogh P. | 01/21/2010 |
| Phenotypic heterogeneity among different vascular elements within distinct anatomical regions of the spleen differentially depends on developmental factors such as lymphotoxin signaling or Nkx2.3, whereas the marginal sinus is controlled by both pathways. | Distinct roles of lymphotoxin-beta signaling and the homeodomain transcription factor Nkx2.3 in the ontogeny of endothelial compartments in spleen.
Balogh P, Balázs M, Czömpöly T, Weih DS, Arnold HH, Weih F. | 01/21/2010 |
| NKX2.3 has a role in mouse pharyngeal organogenesis | NK-2 class homeobox genes and pharyngeal/oral patterning: Nkx2-3 is required for salivary gland and tooth morphogenesis.
Biben C, Wang CC, Harvey RP. | 01/21/2010 |
| Data indicate a substantial role for Nkx2-3 in the correct association of lymphocytes and splenic stromal elements that is independent of chemokine expression. | Architectural defects in the spleens of Nkx2-3-deficient mice are intrinsic and associated with defects in both B cell maturation and T cell-dependent immune responses.
Tarlinton D, Light A, Metcalf D, Harvey RP, Robb L. | 01/21/2010 |