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NKX2.2 is a useful and very sensitive marker for Ewing sarcoma
NKX2.2 demonstrated moderate or strong nuclear positivity in 91.2% of the tumors
nuclear import of Nkx2-2 is mediated not only by the classical import pathway but also directly by imp beta1 or imp 13
NKX2-2 positivity was defined as moderate-to-strong nuclear immunoreactivity in at least 5% of cells
Our study suggests that CGT expression is controlled by balanced expression of the negative modulator OLIG2 and positive regulator Nkx2.2, providing new insights into how expression of GalCer is tightly regulated in cell-type- and stage-specific manners.
lentiviral overexpression of transcription factors ASCL1, SOX10, and NKX2.2 in NPCs was sufficient to induce Sox10 enhancer activity, OPC mRNA, and protein expression consistent with OPC fate
NKX2-2 and MNX1 are etiological genes for neonatal diabetes.
NKX2.2 is a valuable marker for Ewing sarcoma, with a sensitivity of 93% and a specificity of 89%, and aids in the differential diagnosis of small round cell tumors.
The NKX2-2 can induce desired neuronal lineages from most expressing neural progenitor cells by a mechanism resembling developmental binary cell-fate switching.
NKX2-1, NKX2-2, and MEF2C define oncogenic pathways in T cell acute lymphoblastic leukemia (T-ALL).
expression may assist in the determination of the primary tumor site in patients with neuroendocrine tumor metastases of unknown origin: negative would suggest a bronchopulmonary primary, whereas positive would suggest a gastrointestinal primary
Functional analysis revealed that NKX2.2 is an EWS/FLI-regulated gene that is necessary for oncogenic transformation in Ewing's sarcoma.
EWS/FLI mediates transcriptional repression via NKX2.2 during oncogenic transformation in Ewing's sarcoma
NKX2.2 functions in immature endocrine cells to control neuroendocrine differentiation in normal intestine and is expressed in most neuroendocrine tumors of the gut
several genes that are known to be regulated by DNA methylation were up-regulated dramatically by integrin alpha6beta4 expression, including S100A4, FST, PDLIM4, CAPG, and Nkx2.2.
The transient hypoxia at P7 altered the expression of Nkx2.2, resulting in delayed myelination in the external capsule.
This suggests that Nkx2.2 is not only required in the early pancreatic progenitors, but has additional essential activities within the endocrine progenitor population.
Lmx1a is expressed in enterochromaffin cells and functions downstream of Nkx2.2.
Demonstrate that a rare mature enteroendocrine cell subpopulation that is demarcated by Nkx2.2 expression display stem cell properties during normal intestinal epithelial homeostasis, but is not easily activated upon injury.
that Nkx2.2 and Nkx2.9 proteins play no role in the development of branchiovisceral motor neurons in hindbrain rostral to rhombomere 4.
These data identify Nkx2.2 as key regulator to determine neuronal subtypes in the p3 domain of the central nervous system.
The study demonstrates a previously unrecognized mechanism that controls insulin expression through c-Abl-regulated NKx2.2 and GLUT2.
Our studies reveal that a subset of mouse perineurial cells are CNS-derived, express Nkx2.2, and are essential for motor nerve development.
Nato3 induces ectopic Foxa2-positive cells and indirectly downregulates Nkx2.2 expression.
Nkx2.2 functions as a major 'switch' to turn off Pdgfra signaling in oligodendrocyte precursor cells and initiate the intrinsic program for oligodendrocyte differentiation.
Nkx2.2 must repress Neurod1 in a Pdx1+ pancreatic progenitor population to appropriately commit a subset of Neurog3+ endocrine progenitor cells to the alpha cell lineage.
Sirt2 enhances CG4 oligodendroglial differentiation and report a novel mechanism through which Nkx2.2 represses CG4 oligodendroglial differentiation via Sirt2.
Nkx2.2 acts by reinforcing the transcriptional networks initiated by Pax4 and Arx in early committed beta- and alpha-cell, respectively.
Mutation of the endogenous Nkx2.2 tinman (TN) domain in mice abolishes the interaction between Nkx2.2 and Grg3 and disrupts beta-cell specification
these experiments identify novel genetic interactions between Nkx2.2 and Arx within the endocrine progenitor cells that ensure the correct specification and regulation of endocrine hormone-producing cells
sonic hedgehog-GLI1 downstream target genes PTCH1, Cyclin D2, Plakoglobin, PAX6 and NKX2.2 are differently regulated in medulloblastoma and astrocytoma
Data argue that the Nkx2.2 and Nkx2.9 transcription factors contribute crucially to the formation of neuronal networks that function as central pattern generators for locomotor activity in the spinal cord.
nkx2.2a plays a pivotal role in the development of the pancreatic ducts.
Nkx2.2 promotes timely specification and differentiation of myelinating oligodendrocyte lineage cells from species representing different vertebrate taxa.
Nkx2.2 coordinately activates NeuroD1 with Ngn3 in the endocrine progenitor cell and plays a role in the maintenance of NeuroD1 expression to regulate beta cell function in the mature islet.
The protein encoded by this gene contains a homeobox domain and may be involved in the morphogenesis of the central nervous system. This gene is found on chromosome 20 near NKX2-4, and these two genes appear to be duplicated on chromosome 14 in the form of TITF1 and NKX2-8. The encoded protein is likely to be a nuclear transcription factor.
NK2 transcription factor related, locus 2
, homeobox protein XENK-2
, NK-2 homolog B
, NK2 transcription factor-like protein B
, homeobox protein NK-2 homolog B
, homeobox protein Nkx-2.2
, Drosophila NK2 transcription factor related, locus 2
, glycoprotein GP330, renal
, homeobox protein Nkx2-2
, homeobox protein NK-2 homolog B-A
, homeobox protein Nkx-2.2a