Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
Study showed that SHOX2 methylation levels in adenomas and colorectal carcinomas (CRC (show CALR Proteins)) were significantly higher compared to those in normal control tissues. Histologic transition from adenomas to CRC (show CALR Proteins) was paralleled by amplification of the SEPT9 (show SEPT9 Proteins) gene locus.
Study found SHOX2 and SEPT9 (show SEPT9 Proteins) 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 (show NKX2-3 Proteins) and LRRC17 (show LRRC17 Proteins) in myofibroblasts and SHOX2 and TBX5 (show TBX5 Proteins) 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 (show HELLS Proteins) identified 66% of the patients with cancer subsequent to a cytological equivocal diagnosis. SHOX2 complements the cytological diagnosis and the methylation marker panel.
miR (show MLXIP Proteins)-375/SHOX2 functional relationship regulates breast tumorigenesis by controlling the process of EMT (show ITK Proteins).
SHOX2, like SHOX (show SHOX Proteins), regulates NPPB (show BNP Proteins) directly whilst activates ACAN (show ACAN Proteins) via its cooperation with the SOX (show PIPOX Proteins) trio (show TRIO Proteins).
prognostic value of SHOX2 and SEPT9 (show SEPT9 Proteins) DNA methylation (show HELLS Proteins) in benign, paramalignant and malignant pleural effusions
This study shows that expressing human SHOX (show SHOX Proteins) in Shox2SHOX KI/KI (show AXIN1 Proteins) 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 (show TH Proteins)) nerves and the facial motor nucleus
the Shox2-Nkx2-5 (show NKX2-5 Proteins) 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 (show HOXD9 Proteins) and Hoxa11 (show HOXA11 Proteins) expression, juxtaposing the distal expression of Hoxa13 (show HOXA13 Proteins) and Hoxd13 (show HOXD13 Proteins).
study suggested that a certain concentration of FA causes the bone marrow toxicity by regulating the expression of Prx3 (show PRDX3 Proteins)
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 (show SMAD1 Proteins)-dependent pathway to drive tissue growth and to induce Hcn4 (show HCN3 Proteins) expression
phosphorylation essential for repression of Nkx2.5 (show NKX2-5 Proteins) expression during sinoatrial node development and differentiation
These data extend our understanding of the role and regulation of Tbx4 (show TBX4 Proteins) and Shox2 in limb development and limb associated diseases.
Although human SHOX (show SHOX Proteins) can exert similar functions to mouse Shox2 in regulating early temporomandibular joint development, it apparently has a distinct function in the regulation of those molecules that are involved in tissue homeostasis.
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