Affinage

NKX2-3

Homeobox protein Nkx-2.3 · UniProt Q8TAU0

Length
364 aa
Mass
38.4 kDa
Annotated
2026-04-29
42 papers in source corpus 23 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NKX2-3 is a homeodomain transcription factor that governs vascular identity, stromal organization, and organ-specific cell differentiation in the gut, spleen, and associated lymphoid tissues. It directly activates MAdCAM-1 transcription in specialized endothelial cells to control leukocyte homing via α4β7 integrin and L-selectin, and its absence causes splenic vasculature to adopt a peripheral lymph-node-like identity with ectopic high endothelial venules and aberrant lymphatic differentiation (PMID:10790368, PMID:21593383, PMID:37091975). Functioning cell-autonomously in stromal/mesenchymal cells rather than hematopoietic cells, NKX2-3 regulates BMP-2/4 expression in gut mesenchyme to support epithelial proliferation, specifies mucous acinar cell identity in salivary glands, drives marginal-zone B-cell expansion through Lyn/Syk-dependent BCR signaling when ectopically expressed in B cells, and inhibits vascular smooth muscle cell proliferation via AMPK/mTOR-mediated autophagy (PMID:10207146, PMID:12682228, PMID:27297662, PMID:33928642, PMID:38311164). A nonsense mutation in NKX2-3 cosegregates with familial idiopathic intestinal varices in humans (PMID:31498527).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1999 High

    Establishing that NKX2-3 controls intestinal development non-cell-autonomously through mesenchymal BMP signaling resolved how a mesenchyme-expressed transcription factor influences epithelial proliferation.

    Evidence Targeted Nkx2-3 knockout in mice with histological and RT-PCR analysis of BMP-2/4

    PMID:10207146

    Open questions at the time
    • Direct transcriptional targets in gut mesenchyme beyond BMP-2/4 not identified
    • Mechanism by which NKX2-3 activates BMP gene expression not resolved
  2. 2000 High

    Identifying MAdCAM-1 as a direct transcriptional target of NKX2-3 explained how this transcription factor controls leukocyte homing to mucosal tissues and spleen.

    Evidence Nkx2-3 KO mice lack MAdCAM-1; direct promoter activation assay confirmed NKX2-3 binds and activates MAdCAM-1 promoter, replicated across two independent labs

    PMID:10790368 PMID:10926756

    Open questions at the time
    • Co-factors required for MAdCAM-1 activation not identified
    • Whether NKX2-3 is sufficient to induce MAdCAM-1 in non-endothelial contexts unknown
  3. 2002 Medium

    Demonstrating that Nkx2-3 loss causes salivary gland and molar cusp defects expanded the gene's developmental role beyond gut and spleen to oral structures.

    Evidence Histological examination of Nkx2-3 null mice showing sublingual gland and molar defects

    PMID:12141427

    Open questions at the time
    • Downstream targets in salivary gland and dental tissues not identified at this stage
    • Mechanism linking NKX2-3 to cusp morphogenesis unknown
  4. 2003 High

    Bone marrow reconstitution experiments demonstrated that NKX2-3 functions cell-autonomously in stromal cells—not hematopoietic cells—to organize splenic architecture and support marginal-zone B cells.

    Evidence Reciprocal bone marrow transplantation in Nkx2-3−/− mice

    PMID:12682228

    Open questions at the time
    • Identity of the specific stromal cell subset expressing NKX2-3 not defined
    • Stromal signals downstream of NKX2-3 that maintain MZ B cells not identified
  5. 2007 Medium

    Dissecting splenic vascular patterning revealed that NKX2-3 and LTβR signaling operate through distinct pathways—NKX2-3 controls red pulp vascular compartmentalization while LTβR controls marginal sinus maturation.

    Evidence Immunohistochemistry comparing Nkx2-3 KO, LTβR KO, and pharmacological LTβR blockade in mice

    PMID:17318587 PMID:17922052

    Open questions at the time
    • Whether NKX2-3 and LTβR converge on shared downstream effectors not tested
    • Fibroblast subset identities controlled by NKX2-3 not molecularly resolved
  6. 2011 High

    Discovering that Nkx2-3 loss reprograms splenic vasculature to a lymph-node-like identity (HEVs expressing PNAd/CCL21 replacing MAdCAM-1) established NKX2-3 as a master suppressor of alternative vascular fates, with functional consequences for lymphocyte recirculation and pathogen clearance.

    Evidence mRNA profiling, immunohistochemistry, adoptive transfer, and LTβR-blocking experiments in Nkx2-3 KO mice; also detection of aberrant LYVE-1+ endothelial cysts lacking full lymphatic commitment

    PMID:21593383 PMID:21705651

    Open questions at the time
    • Direct transcriptional targets mediating vascular identity suppression not identified
    • Whether vascular reprogramming is reversible upon NKX2-3 restoration unknown
  7. 2011 Medium

    NKX2-3 knockdown in human intestinal microvascular endothelial cells revealed regulation of VEGF-PI3K/AKT-eNOS and endothelin-1 pathways, and NFAT1 was identified as a regulator of NKX2-3 expression through SNP-dependent promoter binding.

    Evidence shRNA knockdown in HIMECs with microarray/RT-PCR; biotin-oligonucleotide pulldown and ChIP for NFAT1 binding at rs11190140

    PMID:21637825 PMID:21803625

    Open questions at the time
    • Functional validation of NFAT1-NKX2-3 axis in vivo not performed
    • Contribution of individual downstream targets (VEGF, EDN1) to NKX2-3-dependent vascular phenotypes not dissected
  8. 2016 High

    Transgenic NKX2-3 overexpression in B cells was sufficient to drive marginal-zone expansion and lymphomagenesis through activation of BCR signaling (Lyn/Syk phosphorylation → NF-κB and PI3K-AKT), revealing an oncogenic gain-of-function mechanism distinct from its stromal role.

    Evidence Transgenic mouse model with NKX2-3 in B cells, phosphorylation assays, migration/homing assays, combined with Nkx2-3 KO analysis

    PMID:27297662

    Open questions at the time
    • Whether NKX2-3 directly activates BCR pathway genes transcriptionally or acts indirectly not resolved
    • Relevance to human marginal-zone lymphoma not genetically confirmed
  9. 2018 Medium

    Placing NKX2-3 downstream of EDA/EDAR signaling and upstream of p21/BMP2/BMPR2 in enamel knot formation defined a developmental signaling cascade for tooth cusp morphogenesis.

    Evidence Microarray in mouse embryos, EDA signaling assays, immunostaining, and Nkx2-3 KO phenotyping

    PMID:30089653

    Open questions at the time
    • Direct promoter binding of NKX2-3 at p21 or BMP2 loci not demonstrated
    • Whether this pathway operates in human dental development untested
  10. 2019 High

    Three advances converged: NKX2-3 was localized to VAP-1+ pericryptal stromal cells in the colon where its absence attenuates colitis; it was shown to control addressin balance in Peyer's patch HEVs; and a human loss-of-function mutation was linked to familial intestinal varices, translating the murine vascular phenotype to human disease.

    Evidence LacZ reporter, bone marrow transplantation, DSS colitis model (PMID:30700585); immunofluorescence and in vivo blocking in Peyer's patches (PMID:25320278); whole-exome sequencing with LOD 3.3 in a four-generation pedigree (PMID:31498527)

    PMID:25320278 PMID:30700585 PMID:31498527

    Open questions at the time
    • Precise stromal cell-derived signals mediating colitis promotion not identified
    • Functional validation of the human nonsense mutation (e.g., rescue) not performed
    • Whether NKX2-3 variants contribute to common IBD pathogenesis mechanistically remains unclear
  11. 2020 Medium

    Demonstrating that NKX2-3 promotes VSMC autophagy via AMPK/mTOR to inhibit proliferation and migration extended NKX2-3 function to vascular remodeling and suggested therapeutic relevance for neointima formation.

    Evidence Adenoviral overexpression/siRNA KD in VSMCs, carotid balloon injury model, autophagy inhibitor (3-MA) rescue in vivo and in vitro

    PMID:33928642

    Open questions at the time
    • Direct transcriptional targets linking NKX2-3 to AMPK activation not identified
    • Whether this mechanism operates in human vascular disease not tested
  12. 2023 Medium

    Revealing that Nkx2-3 loss leads to ectopic splenic lymphatic capillaries and impaired splenic erythropoiesis/megakaryopoiesis deepened the understanding of NKX2-3 as a gatekeeper of venous versus lymphatic endothelial fate in the spleen.

    Evidence Immunofluorescence, flow cytometry, qPCR, and Romiplostim stimulation in Nkx2-3 KO mice

    PMID:37091975

    Open questions at the time
    • Whether the erythropoietic defect is secondary to vascular changes or reflects an independent stromal function unknown
    • Transcriptional program suppressing lymphatic commitment not defined
  13. 2024 Medium

    NKX2-3 was identified as a key specifier of mucous acinar cell identity in salivary glands and as a regulator of PLVAP/SPARCL1 in pancreatic endothelial cells, broadening its role as a tissue-specific transcriptional organizer of specialized cell fates.

    Evidence RNAseq and proteomics of Nkx2.3 KO salivary glands (PMID:38311164); NKX2-3 transfection in HUVECs with RT-qPCR and motif analysis (PMID:39445426)

    PMID:38311164 PMID:39445426

    Open questions at the time
    • Direct NKX2-3 binding at mucous acinar gene promoters not confirmed by ChIP
    • PLVAP induction by NKX2-3 not validated in native pancreatic endothelial cells

Open questions

Synthesis pass · forward-looking unresolved questions
  • The genome-wide direct target repertoire of NKX2-3 remains undefined in any tissue; no ChIP-seq dataset exists, the cofactors mediating its context-dependent transcriptional activity are unknown, and its structural basis for DNA recognition specificity versus other NKX family members has not been resolved.
  • No ChIP-seq or CUT&RUN data defining direct genome-wide binding in any cell type
  • Cofactors or chromatin remodelers partnering with NKX2-3 not identified
  • Structural basis for tissue-specific target selection unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 9 GO:0003677 DNA binding 3
Localization
GO:0005634 nucleus 5
Pathway
R-HSA-74160 Gene expression (Transcription) 8 R-HSA-168256 Immune System 6 R-HSA-1266738 Developmental Biology 4 R-HSA-162582 Signal Transduction 3 R-HSA-9612973 Autophagy 1
Partners
BMP2BMP4FLI1MADCAM1NFAT1PLVAPPTPN2

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 Targeted inactivation of Nkx2-3 in mice causes delayed villus formation in small intestine due to reduced epithelial proliferation, and reduced BMP-2 and BMP-4 expression in gut mesenchyme, suggesting non-cell-autonomous control of intestinal cell growth through BMP signaling downstream of Nkx2-3. Targeted gene knockout in mice with histological and molecular phenotyping (RT-PCR for BMP-2/4), and observation of intestinal and splenic defects Development (Cambridge, England) High 10207146
2000 NKX2-3 directly activates MAdCAM-1 transcription in spleen and mucosa-associated lymphoid tissue endothelial cells; NKX2-3-deficient mice completely lack MAdCAM-1, and this loss is responsible for the migration and homing defects of lymphocytes and macrophages. Targeted gene knockout in mice, immunohistochemistry, RT-PCR, transcriptional activation assay (direct activation of MAdCAM-1 promoter by NKX2-3) The EMBO journal High 10790368 10926756
2000 Nkx2-3, expressed in visceral mesoderm, controls regional expression of MAdCAM-1 in specialized endothelial cells; loss of Nkx2-3 leads to down-regulation of MAdCAM-1 in endothelial cells where Nkx2-3 is normally expressed, impairing leukocyte homing via L-selectin and α4β7 integrin. Targeted gene knockout, semiquantitative RT-PCR, immunohistochemistry of MAdCAM-1 in Nkx2-3-deficient mice Developmental biology High 10926756
2003 The splenic architectural defects and absence of marginal zone B cells in Nkx2-3-deficient mice are of stromal (non-hematopoietic) origin, as shown by bone marrow reconstitution studies, establishing that Nkx2-3 functions in stromal cells to support correct lymphocyte-stroma interactions. Bone marrow reconstitution (transplantation) experiments in Nkx2-3-/- mice Journal of immunology High 12682228
2007 Nkx2-3 deficiency causes complex organizational defects in white pulp fibroblast subsets in the spleen, including distributional abnormalities and absence of a complementary fibroblast subpopulation, indicating Nkx2-3 controls fibroblast ontogeny in a tissue-specific manner. Immunohistochemistry and dual-label immunofluorescence in Nkx2-3-deficient mice Pathology oncology research Medium 17922052
2007 The splenic vasculature patterning is controlled by two distinct pathways: lymphotoxin-β receptor signaling controls marginal sinus maturation, while Nkx2.3 transcription factor controls vascular compartmentalization of the red pulp and marginal sinus integrity. Immunohistochemistry in Nkx2-3-deficient mice, LTβR-Ig fusion protein blockade, and genetic deletion of LTβR/RelB/p52 Cell and tissue research Medium 17318587
2011 In the absence of Nkx2-3, the spleen develops a peripheral lymph node-like vascular identity, including formation of high endothelial venules (HEVs) expressing PNAd addressin and CCL21, replacing MAdCAM-1; this vascular reprogramming is dependent on lymphotoxin-β receptor signaling and mature T and B cells, impairs lymphocyte recirculation and blood-borne pathogen uptake. Comparative mRNA expression profiling, immunohistochemistry, adoptive lymphocyte transfer, functional blocking experiments in Nkx2-3-deficient mice Journal of immunology High 21593383
2011 Nkx2-3 deficiency in the spleen leads to formation of LYVE-1-positive endothelial cysts without true lymphatic commitment (lacking VEGFR-3 and Prox1), indicating that Nkx2-3 normally suppresses this aberrant endothelial differentiation program. Immunohistochemistry, real-time quantitative PCR, short-term lymphocyte cell-tracing in Nkx2-3-deficient mice The journal of histochemistry and cytochemistry Medium 21705651
2011 NKX2-3 regulates endothelin-1 (EDN1) and VEGF-PI3K/AKT-eNOS signaling pathways in human intestinal microvascular endothelial cells (HIMECs), with NKX2-3 knockdown reducing VEGF/PI3K/AKT/eNOS expression and increasing EDN1, as validated by cDNA microarray and RT-PCR. shRNA knockdown in HIMEC lines, cDNA microarray, RT-PCR validation, pathway analysis PloS one Medium 21637825
2011 NFAT1 differentially binds to the NKX2-3 promoter region containing rs11190140 SNP, with higher binding to non-methylated and methylated C allele than to T allele, as confirmed by biotin-oligonucleotide pulldown and ChIP assay, suggesting NFAT1 regulates NKX2-3 expression. Biotin-labeled oligonucleotide pulldown with nuclear extracts, Western blot, ChIP assay Molecular genetics and metabolism Medium 21803625
2012 NKX2-3 positively regulates PTPN2 expression in B cells and intestinal microvascular endothelial cells; NKX2-3 knockdown reduces PTPN2 mRNA, and mRNA expression of PTPN2 and NKX2-3 are positively correlated in CD patients. siRNA knockdown, cDNA microarray, RT-PCR validation in B cells and HIMECs Disease markers Medium 22377701
2014 Nkx2-3 controls the addressin balance in high endothelial venules of Peyer's patches by maintaining MAdCAM-1 expression; in Nkx2-3-deficient mice, MAdCAM-1 is replaced by PNAd (peripheral node addressin) in an LTβR- and lymphocyte-dependent manner, while general HEV functionality for lymphocyte homing is preserved. Immunofluorescence, flow cytometry, in vivo MECA-79 blocking, quantitative PCR in Nkx2-3-deficient mice Journal of immunology Medium 25320278
2016 NKX2-3 promotes marginal-zone lymphomagenesis by inducing B-cell receptor signaling through phosphorylation of Lyn/Syk kinases, which activate integrins (LFA-1, VLA-4), adhesion molecules (ICAM-1, MAdCAM-1), and CXCR4, ultimately triggering NF-κB and PI3K-AKT pathways; transgenic NKX2-3 overexpression in B cells is sufficient to drive marginal-zone expansion and lymphoma development. Transgenic mouse model (NKX2-3 overexpression in B cells), Nkx2-3-deficient mice, phosphorylation assays, functional migration/homing assays, signaling pathway analysis Nature communications High 27297662
2018 NKX2-3 is a target of EDA/EDAR signaling in the enamel knot; NKX2-3 mediates p21 expression, activates BMP signaling by upregulating Bmp2 and Bmpr2 in dental epithelium, and decreases SOX2 expression, establishing an EDA→NKX2-3→p21/BMP2/BMPR2 pathway required for enamel knot formation and cusp morphogenesis. Gene microarray in mouse embryos, EDA signaling assays, immunostaining, Nkx2-3-deficient mouse phenotyping The Journal of biological chemistry Medium 30089653
2019 BMP2b from pharyngeal ectoderm activates Smad effectors in endodermal cells to induce nkx2.3-positive pharyngeal pouch progenitors in zebrafish; BMP signaling is required for specification of these nkx2.3+ progenitors, which give rise to the pouch epithelium. Cell lineage tracing, transgenic ablation, chemical inhibitor screen, loss-of-function analyses, Smad effector assays in zebrafish PLoS genetics Medium 30763319
2019 Nkx2.3 expression is restricted to VAP-1+ myofibroblast-like pericryptal stromal cells in the colon; Nkx2.3-/- hematopoietic cells cannot rescue wild-type mice from colitis, whereas absence of Nkx2.3 in stromal cells attenuates DSS-induced colitis and enhances colonic epithelial regeneration, placing Nkx2.3 in stromal cells as a driver of colitis. LacZ-Nkx2.3 reporter mice, bone marrow transplantation rescue experiments, DSS colitis model, flow cytometry, quantitative PCR Journal of immunology High 30700585
2019 A nonsense mutation in NKX2-3 cosegregates with familial idiopathic intestinal varices in a four-generation human pedigree (LOD score 3.3), linking NKX2-3 loss-of-function to intestinal vascular development in humans, consistent with the molecular pathway established in mice. Whole-exome sequencing, targeted Sanger sequencing, linkage analysis (LOD score) Human mutation Medium 31498527
2020 Nkx2-3 inhibits proliferation and migration of vascular smooth muscle cells (VSMCs) by promoting autophagy through activation of the AMPK/mTOR signaling pathway; autophagy inhibition with 3-MA abolished the inhibitory effects of Nkx2-3 on VSMC proliferation and migration both in vivo and in vitro. Adenovirus-mediated overexpression and siRNA knockdown, carotid balloon injury model, EdU/CCK-8 proliferation assays, scratch migration assay, fluorescent mRFP-GFP-LC3 autophagy assay, transmission electron microscopy, AMPK/mTOR pathway inhibitor rescue Journal of cellular physiology Medium 33928642
2021 Aberrantly expressed NKX2-3 in a megakaryoblastic AML cell line (ELF-153) activates FLI1, a master factor for myelopoiesis driving megakaryocytic differentiation and suppressing erythroid differentiation, implicating NKX2-3 as an oncogenic driver of specific AML subtypes through FLI1 regulation. Comparative expression profiling, siRNA knockdown experiments in AML cell lines International journal of molecular sciences Medium 34768865
2023 In the absence of Nkx2-3, the spleen develops ectopic Prox1-positive lymphatic capillaries (gp38/CD31 double-positive lymphatic endothelial cells) and loses Clever1-positive venous red pulp segments, resulting in impaired splenic erythropoiesis and severely reduced megakaryocyte colony formation after Romiplostim stimulation. Immunofluorescence, flow cytometry, quantitative PCR, pharmacological stimulation (Romiplostim/thrombopoietin-receptor mimetic) in Nkx2-3-deficient mice Frontiers in cell and developmental biology Medium 37091975
2024 Nkx2.3 is a key regulator of the molecular program specifying mucous acinar cell identity in the sublingual salivary gland; Nkx2.3-/- mice show loss of mucous acinar cell gene expression program as demonstrated by RNAseq, immunostaining, and proteomic analysis of saliva. Targeted gene knockout, RNAseq, immunostaining, proteomic analysis of saliva in Nkx2.3-/- mice Developmental biology Medium 38311164
2024 NKX2-3 acts upstream of PLVAP and SPARCL1 in pancreatic endothelial cells; induction of NKX2-3 in HUVECs promotes expression of PLVAP and SPARCL1, and NKX2-3 binding motifs are found in ~40% of the pancreatic EC signature genes. Gene transfection of NKX2-3 into HUVECs, RT-qPCR, single-cell RNA-sequencing data analysis, DNA-binding motif analysis Arteriosclerosis, thrombosis, and vascular biology Medium 39445426
2002 Nkx2-3 is required for maturation and cellular organization of sublingual salivary glands, and for cusp formation in mandibular molars; loss of Nkx2-3 in null mice results in defects in these oral structures. Examination of Nkx2-3 null mice with histology and expression analysis The International journal of developmental biology Medium 12141427

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1996 A new tinman-related gene, nkx2.7, anticipates the expression of nkx2.5 and nkx2.3 in zebrafish heart and pharyngeal endoderm. Developmental biology 143 8954740
1999 Targeted disruption of the homeobox transcription factor Nkx2-3 in mice results in postnatal lethality and abnormal development of small intestine and spleen. Development (Cambridge, England) 142 10207146
2000 NKX2.3 is required for MAdCAM-1 expression and homing of lymphocytes in spleen and mucosa-associated lymphoid tissue. The EMBO journal 78 10790368
1997 The mouse Nkx2-3 homeodomain gene is expressed in gut mesenchyme during pre- and postnatal mouse development. Developmental dynamics : an official publication of the American Association of Anatomists 59 9142493
2000 Homeodomain factor Nkx2-3 controls regional expression of leukocyte homing coreceptor MAdCAM-1 in specialized endothelial cells of the viscera. Developmental biology 54 10926756
2016 Homeobox NKX2-3 promotes marginal-zone lymphomagenesis by activating B-cell receptor signalling and shaping lymphocyte dynamics. Nature communications 43 27297662
2003 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. Journal of immunology (Baltimore, Md. : 1950) 38 12682228
2002 NK-2 class homeobox genes and pharyngeal/oral patterning: Nkx2-3 is required for salivary gland and tooth morphogenesis. The International journal of developmental biology 36 12141427
2020 Tetramerisation of the CRISPR ring nuclease Crn3/Csx3 facilitates cyclic oligoadenylate cleavage. eLife 31 32597755
2019 BMP signaling is required for nkx2.3-positive pharyngeal pouch progenitor specification in zebrafish. PLoS genetics 25 30763319
2011 NKX2-3 transcriptional regulation of endothelin-1 and VEGF signaling in human intestinal microvascular endothelial cells. PloS one 25 21637825
2018 The transcription factor NKX2-3 mediates p21 expression and ectodysplasin-A signaling in the enamel knot for cusp formation in tooth development. The Journal of biological chemistry 24 30089653
2011 Transcription factor Nkx2-3 controls the vascular identity and lymphocyte homing in the spleen. Journal of immunology (Baltimore, Md. : 1950) 24 21593383
2009 Association of a Nkx2-3 polymorphism with Crohn's disease and expression of Nkx2-3 is up-regulated in B cell lines and intestinal tissues with Crohn's disease. Journal of Crohn's & colitis 24 21172269
2015 Crystal structures of CRISPR-associated Csx3 reveal a manganese-dependent deadenylation exoribonuclease. RNA biology 20 26106927
2010 Genes regulated by Nkx2-3 in sporadic and inflammatory bowel disease-associated colorectal cancer cell lines. Digestive diseases and sciences 20 20165982
2020 Csx3 is a cyclic oligonucleotide phosphodiesterase associated with type III CRISPR-Cas that degrades the second messenger cA4. The Journal of biological chemistry 19 32826317
2012 PTPN2 is associated with Crohn's disease and its expression is regulated by NKX2-3. Disease markers 16 22377701
2021 Nkx2-3 induces autophagy inhibiting proliferation and migration of vascular smooth muscle cells via AMPK/mTOR signaling pathway. Journal of cellular physiology 15 33928642
2011 NKX2-3 variant rs11190140 is associated with IBD and alters binding of NFAT. Molecular genetics and metabolism 15 21803625
2010 Genes regulated by Nkx2-3 in siRNA-mediated knockdown B cells: implication of endothelin-1 in inflammatory bowel disease. Molecular genetics and metabolism 13 20188614
2009 Lack of association of NKX2-3, IRGM, and ATG16L1 inflammatory bowel disease susceptibility variants with celiac disease. Human immunology 13 19683022
2016 Recognition of a pseudo-symmetric RNA tetranucleotide by Csx3, a new member of the CRISPR associated Rossmann fold superfamily. RNA biology 12 26727591
2007 Distinct roles of lymphotoxin-beta signaling and the homeodomain transcription factor Nkx2.3 in the ontogeny of endothelial compartments in spleen. Cell and tissue research 12 17318587
2021 NKL Homeobox Genes NKX2-3 and NKX2-4 Deregulate Megakaryocytic-Erythroid Cell Differentiation in AML. International journal of molecular sciences 11 34768865
2019 Mutations in RPSA and NKX2-3 link development of the spleen and intestinal vasculature. Human mutation 11 31498527
2014 Contribution of NKX2-3 polymorphisms to inflammatory bowel diseases: a meta-analysis of 35358 subjects. Scientific reports 11 24473197
2014 Absence of Nkx2-3 homeodomain transcription factor reprograms the endothelial addressin preference for lymphocyte homing in Peyer's patches. Journal of immunology (Baltimore, Md. : 1950) 11 25320278
2020 Ameliorated Autoimmune Arthritis and Impaired B Cell Receptor-Mediated Ca2+ Influx in Nkx2-3 Knock-out Mice. International journal of molecular sciences 9 32859051
2011 Increased expression of NKX2.3 mRNA transcribed from the risk haplotype for ulcerative colitis in the involved colonic mucosa. Human immunology 9 21514341
2011 Absence of Nkx2-3 homeodomain transcription factor induces the formation of LYVE-1-positive endothelial cysts without lymphatic commitment in the spleen. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 8 21705651
2019 IL-22-Independent Protection from Colitis in the Absence of Nkx2.3 Transcription Factor in Mice. Journal of immunology (Baltimore, Md. : 1950) 7 30700585
2012 Genes differentially regulated by NKX2-3 in B cells between ulcerative colitis and Crohn's disease patients and possible involvement of EGR1. Inflammation 7 21968973
2007 Complex organizational defects of fibroblast architecture in the mouse spleen with Nkx2.3 homeodomain deficiency. Pathology oncology research : POR 6 17922052
2024 Single-Cell Meta-Analysis Uncovers the Pancreatic Endothelial Cell Transcriptomic Signature and Reveals a Key Role for NKX2-3 in PLVAP Expression. Arteriosclerosis, thrombosis, and vascular biology 5 39445426
2021 Identification of novel, clonally stable, somatic mutations targeting transcription factors PAX5 and NKX2-3, the epigenetic regulator LRIF1, and BRAF in a case of atypical B-cell chronic lymphocytic leukemia harboring a t(14;18)(q32;q21). Cold Spring Harbor molecular case studies 3 33608382
2025 Ethanol Induces Craniofacial Defects in Bmp Mutants Independent of nkx2.3 by Elevating Cranial Neural Crest Cell Apoptosis. Biomedicines 2 40149732
2023 Absence of Nkx2-3 induces ectopic lymphatic endothelial differentiation associated with impaired extramedullary stress hematopoiesis in the spleen. Frontiers in cell and developmental biology 2 37091975
2024 Nkx2.3 transcription factor is a key regulator of mucous cell identity in salivary glands. Developmental biology 1 38311164
2025 Ethanol induces craniofacial defects in Bmp mutants independent of nkx2.3 by elevating cranial neural crest cell apoptosis. bioRxiv : the preprint server for biology 0 39803440
2025 Nkx2-3 Homeobox Gene Plays an Essential Role in Later Stages of Orofacial Differentiation. Annals of pediatrics & child health 0 40416342
2023 Quantitative Analysis of NKX2-3 Expression in Human Colon: An Immunohistochemical Study. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 0 38063211