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High SHOX2 methylation is associated with Lung cancer.
Data suggest that the microRNA miR (zeige MLXIP Antikörper)-375/short stature homeobox 2 protein (SHOX2) axis may be a novel therapeutic target for esophageal squamous cell carcinoma (ESCC).
Study showed that SHOX2 methylation levels in adenomas and colorectal carcinomas (CRC (zeige CALR Antikörper)) were significantly higher compared to those in normal control tissues. Histologic transition from adenomas to CRC (zeige CALR Antikörper) was paralleled by amplification of the SEPT9 (zeige SEPT9 Antikörper) gene locus.
Study found SHOX2 and SEPT9 (zeige SEPT9 Antikörper) frequently methylated in biliary tract cancers.
We have identified that SHOX2 expression or methylation are potent independent prognostic indicators for predicting LGG patient survival, and have potential to identify an important subset of LGG patients with IDHwt status with significantly better overall survival.
Whole-genome microarray mRNA-expression profiles of myofibroblasts and skin fibroblasts revealed four additional genes that are significantly differentially expressed in these two cell types: NKX2-3 (zeige NKX2-3 Antikörper) and LRRC17 (zeige LRRC17 Antikörper) in myofibroblasts and SHOX2 and TBX5 (zeige TBX5 Antikörper) in skin fibroblasts
these results suggest a genetic contribution of SHOX2 in early-onset atrial fibrillation
SHOX2 overexpression favors differentiation of embryonic stem cells into cardiac pacemaker cells, improving biological pacing ability.
SHOX2 DNA methylation (zeige HELLS Antikörper) identified 66% of the patients with cancer subsequent to a cytological equivocal diagnosis. SHOX2 complements the cytological diagnosis and the methylation marker panel.
miR (zeige MLXIP Antikörper)-375/SHOX2 functional relationship regulates breast tumorigenesis by controlling the process of EMT (zeige ITK Antikörper).
Shox2 patterns the stylopod as a repressor via interaction with enhancers active in the proximal limb mesenchyme and antagonizes the repressive function of TALE factors in osteogenesis.
This study shows that expressing human SHOX (zeige SHOX Antikörper) in Shox2SHOX KI/KI (zeige AXIN1 Antikörper) mice leads to congenital osteoarthritislike disease of the temporomandibular joint in postnatal mice. This provides a novel in vivo model for studying the molecular and cellular mechanisms of temporomandibular joint osteoarthritis.
Results demonstrate that elimination of Shox2 in the brain results in disruptions in the development of the facial (VII (zeige TH Antikörper)) nerves and the facial motor nucleus
the Shox2-Nkx2-5 (zeige NKX2-5 Antikörper) antagonistic mechanism primes the pacemaker cell fate in the pulmonary vein myocardium and sinoatrial node
Shox2 expression restricted to the proximal limb along with Hoxd9 (zeige HOXD9 Antikörper) and Hoxa11 (zeige HOXA11 Antikörper) expression, juxtaposing the distal expression of Hoxa13 (zeige HOXA13 Antikörper) and Hoxd13 (zeige HOXD13 Antikörper).
study suggested that a certain concentration of FA causes the bone marrow toxicity by regulating the expression of Prx3 (zeige PRDX3 Antikörper)
Data indicate the importance of short stature homeobox 2 (Shox2) in the cerebellum.
Shox2 regulates dorsal mesenchymal protrusion fate and development by controlling BMP signaling through the Smad (zeige SMAD1 Antikörper)-dependent pathway to drive tissue growth and to induce Hcn4 (zeige HCN3 Antikörper) expression
phosphorylation essential for repression of Nkx2.5 (zeige NKX2-5 Antikörper) expression during sinoatrial node development and differentiation
These data extend our understanding of the role and regulation of Tbx4 (zeige TBX4 Antikörper) and Shox2 in limb development and limb associated diseases.
Shox2 deficiency interferes with pacemaking function in zebrafish embryos. Shox2 has a critical function in the recruitment of sinus venosus myocardium comprising the sinoatrial nodal region.
This gene is a member of the homeobox family of genes that encode proteins containing a 60-amino acid residue motif that represents a DNA binding domain. Homeobox genes have been characterized extensively as transcriptional regulators involved in pattern formation in both invertebrate and vertebrate species. Several human genetic disorders are caused by aberrations in human homeobox genes. This locus represents a pseudoautosomal homeobox gene that is thought to be responsible for idiopathic short stature, and it is implicated in the short stature phenotype of Turner syndrome patients. This gene is considered to be a candidate gene for Cornelia de Lange syndrome. Alternative splicing results in multiple transcript variants.
short stature homeobox 2
, SHOX homologous gene on chromosome 3
, homeobox protein Og12X
, paired-related homeobox protein SHOT
, short stature homeobox protein 2
, paired family homeodomain protein Prx3