Enhancer ID: | E_02_0517 |
Species: | human |
Position : | chr8:66917733-66919733 |
Biosample name: | |
Experiment class : | High+Lowthroughput |
Enhancer type: | Enhancer |
Disease: | Gastric cancer |
Pubmed ID: | 30031062 |
Enhancer experiment: | QRT PCR, immunohistochemical staining, Western blot, rna-fish, statistical analysis |
Enhancer experiment description: | Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers. Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21. H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6]. |
Target gene : | SNHG6,EZH2,H19,XIST |
Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
Less strong evidence: | RNA-Seq |
Target gene experiment description: | Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers. Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21. H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].;Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers. Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21. H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].;Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers. Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21. H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].;Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers. Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21. H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6]. |
TF name : | -- |
TF experiment: | qRT-PCR,Immunohistochemical staining,western blot,RNA-FISH,???? |
TF experiment description: | Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers. Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21. H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].;Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers. Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21. H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].;Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers. Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21. H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].;Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers. Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21. H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6]. |
Enhancer function : | Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers. Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21. H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6]. |
Enhancer function experiment: | Immunohistochemical staining |
Enhancer function experiment description: |
Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers. Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21. H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6]. |
SNP ID: | -- |
GeneName | Pathway Name | Source | Gene Number |
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