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The DNA-associated protein encoded by PHOX2B is a member of the paired family of homeobox proteins localized to the nucleus. Additionally we are shipping PHOX2B Antibodies (54) and PHOX2B Proteins (2) and many more products for this protein.
reduced dosage of PHOX2B during development, through either a heterozygous deletion or dominant-negative mutation, imposes a block in the differentiation of sympathetic neuronal precursors
Phox2b is expressed throughout the primary taste centers of two cyprinid fish, Danio rerio and Carassius auratus
Phox2b function is sox10 (show SOX10 ELISA Kits)-dependent in the developing enteric nervous system
The discovery of gain-of-function mutations in the ALK (show ALK ELISA Kits) receptor tyrosine kinase (show RET ELISA Kits) gene as the major cause of familial neuroblastoma (show ARHGEF16 ELISA Kits) led to the discovery of identical somatic mutations and rapid advancement of ALK (show ALK ELISA Kits) as a tractable therapeutic target. Inactivating mutations in a master regulator of neural crest development, PHOX2B, have also been identified in a subset of familial neuroblastomas.
Given the association between congenital heart disease and aberrant neural crest cell development, however, findings are suggestive that congenital heart disease may be a rare feature of PHOX2B mutation which has not been previously reported
This study is the first to evaluate minimal residual disease detection using neuroblastoma (show ARHGEF16 ELISA Kits) mRNAs in human ovarian tissue. Only PHOX2B was a reliable marker of neuroblastoma (show ARHGEF16 ELISA Kits) cells contaminating ovarian tissue.
This truncated protein localized to the nucleus and transactivated a target promoter. These data suggest that nonsense pathogenic variants in the first exon of PHOX2B likely escape nonsense mediated decay (NMD) and produce N-terminally truncated proteins functionally distinct from those produced by the more common polyalanine repeat mutations (PARMs).
These pre-clinical data strongly suggest that PHOX2B functions as a suppressor of neuroblastoma (show ARHGEF16 ELISA Kits) progression.
High PHOX2B expression is associated with Neuroblastoma (show ARHGEF16 ELISA Kits).
PHOX2B forms homodimers and heterodimerizes weakly with mutated proteins, excluding the direct involvement of the polyalanine tract in dimer formation, indicating that mutated proteins retain partial ability to form heterodimers with PHOX2A (show PHOX2A ELISA Kits).
Expression of NOX4 (show NOX4 ELISA Kits)/p22(phox (show CYBA ELISA Kits)) as well as ROS (show ROS1 ELISA Kits) production is enhanced by IL-1beta (show IL1B ELISA Kits). On the other hand, the use of NOX4 (show NOX4 ELISA Kits) inhibitors decreased IL-1beta (show IL1B ELISA Kits)-induced collagenase synthesis by chondrocytes.
PHOX2A (show PHOX2A ELISA Kits) expression is finely controlled during retinoic acid differentiation and this, together with PHOX2B down-regulation.
Point "silent" mutations affecting different nucleotides of the PHOX2B gene were observed in 32 % of patients with Class III malocclusion and never in controls (0 %).
Murine models of congenital central hypoventilation syndrome designed with PHOX2B mutations have suggested RTN neuron agenesis.
The retrotrapezoid nucleus neurons expressing Atoh1 (show ATOH1 ELISA Kits) and Phox2b are essential for the respiratory response to CO2.
Adult Phox2b(+/-) mice showed altered exploratory behavior in the open field and in the elevated plus maze, both indicative of anxiety. Phox2b(+/-) mice did not show cognitive or motor impairments.
many cranial nerve-associated crest cells coexpress the pan-autonomic determinant Paired-like homeodomain 2b (Phox2b) together with markers of Schwann cell precursors. Some give rise to Schwann cells after down-regulation of PHOX2b.
In this review, conditional mouse mutants of Phox2b(27Ala) lacked the ventilary response to hypercapnia at birth.
Phox2b transcripts were identified in FAC (show FANCC ELISA Kits)-sorted Pitx3 (show PITX3 ELISA Kits) positive neurons.
This study demonistrated that Phox2b-expressing retrotrapezoid neurons are intrinsically responsive to H+ and CO2.
Nonpolyalanine repeat expansion mutation of PHOX2B is both a dominant-negative and gain-of-function mutation.
The PHOX2B can induce desired neuronal lineages from most expressing neural progenitor cells by a mechanism resembling developmental binary cell-fate switching.
The cranial sensory pathways, somatic and visceral, are related, and Phox2b serves as a developmental switch from the former to the latter.
The DNA-associated protein encoded by this gene is a member of the paired family of homeobox proteins localized to the nucleus. The protein functions as a transcription factor involved in the development of several major noradrenergic neuron populations and the determination of neurotransmitter phenotype. The gene product is linked to enhancement of second messenger-mediated activation of the dopamine beta-hydroylase, c-fos promoters and several enhancers, including cyclic amp-response element and serum-response element.
paired-like homeobox 2b
, paired mesoderm homeobox protein 2B
, PHOX2B homeodomain protein
, neuroblastoma Phox
, neuroblastoma paired-type homeobox protein
, paired mesoderm homeobox 2b
, GENA 269
, dilated pupils 1