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SHOX2 and PTGER4 methylation detection in blood plasma has certain value in the early diagnosis of lung cancer
Post-therapeutic SHOX2 and SEPT9 circulating cell-free DNA(ccfDNA) methylation levels correlated with UICC stage (all P <0.01). SEPT9 ccfDNA methylation further allowed for an accurate pre- and post-therapeutic detection of distant metastases.
the first report on the association of SHOX2 loss-of-function mutation with enhanced susceptibility to familial Atrial fibrillation
the methylation positive rates of SHOX2 with RASSF1A in stage III were both higher than the other stages of lung cancer
High SHOX2 methylation is associated with Lung cancer.
important role in the process of intervertebral disc degeneration
Data suggest that the microRNA miR-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) were significantly higher compared to those in normal control tissues. Histologic transition from adenomas to CRC was paralleled by amplification of the SEPT9 gene locus.
Study found SHOX2 and SEPT9 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 and LRRC17 in myofibroblasts and SHOX2 and TBX5 in skin fibroblasts
these results suggest a genetic contribution of SHOX2 in early-onset atrial fibrillation
The longitudinal measurement of extracellular plasma mSHOX2 DNA yields information about the response to cytotoxic treatment and allows an early assessment of treatment response for lung cancer patients.
SHOX2 overexpression favors differentiation of embryonic stem cells into cardiac pacemaker cells, improving biological pacing ability.
SHOX2 DNA methylation identified 66% of the patients with cancer subsequent to a cytological equivocal diagnosis. SHOX2 complements the cytological diagnosis and the methylation marker panel.
miR-375/SHOX2 functional relationship regulates breast tumorigenesis by controlling the process of EMT.
SHOX2, like SHOX, regulates NPPB directly whilst activates ACAN via its cooperation with the SOX trio.
prognostic value of SHOX2 and SEPT9 DNA methylation in benign, paramalignant and malignant pleural effusions
Elevated SHOX2 expression is associated with tumor recurrence of hepatocellular carcinoma.
The combination of EBUS-TBNA and SHOX2 methylation level strongly improves the assessment of the nodal status by identifying additional malignant lesions and confirming benign nodes and therefore avoiding invasive follow-up procedures.
gap junctional coupling promotes synchronization of Shox2 interneurons, and may be implicated in locomotor rhythmicity in developing mice.
Shox2(+/+) and Shox2(-/-) embryonic stem cell clones were isolated and differentiated according to five different protocols in order to evaluate the most efficient enrichment of sinoatrial node-like cells. .
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 in Shox2SHOX KI/KI 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.
Electric-pulse current stimulation (EPCS) promotes the differentiation of mShox2 genetically modified canine mesenchymal stem cells (cMSCs) into pacemaker-like cells, which generates more If current.
Results demonstrate that elimination of Shox2 in the brain results in disruptions in the development of the facial (VII) nerves and the facial motor nucleus
the Shox2-Nkx2-5 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 and Hoxa11 expression, juxtaposing the distal expression of Hoxa13 and Hoxd13.
study suggested that a certain concentration of FA causes the bone marrow toxicity by regulating the expression of Prx3
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-dependent pathway to drive tissue growth and to induce Hcn4 expression
phosphorylation essential for repression of Nkx2.5 expression during sinoatrial node development and differentiation
These data extend our understanding of the role and regulation of Tbx4 and Shox2 in limb development and limb associated diseases.
Although human SHOX 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 regulates progression through chondrogenesis at two distinct stages--the onset of early differentiation and the transition to maturation and hypertrophy.
both hSHOX and mShox2 limb enhancers are coupled to distinct neural enhancers. This is the first report demonstrating the activity of cis-regulatory elements from the hSHOX and mShox2 genomic regions in mammalian embryos.
Optogenetic silencing or blocking synaptic output of Shox2 interneurons in transgenic mice perturbed rhythm without an effect on pattern generation
Shox2 can regulate the expression of Adrb3 and control the rate of lipolysis and, in this way, exerts control of the phenotypic differences between visceral and s.c. adipocytes
Our findings demonstrate a novel epistatic relationship between Shox2 and Isl1 in the heart with important developmental consequences for sinoatrial node formation and heart beat.
Hoxa11 and Hoxd11 regulate chondrocyte differentiation upstream of Runx2 and Shox2 in mice.
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