|
Spinal Muscular Atrophy
|
0.100 |
Biomarker
|
disease |
BEFREE |
Reduced expression of the survival motor neuron (SMN) protein causes the neurodegenerative disease spinal muscular atrophy (SMA).
|
31851921 |
2019 |
|
Neurodegenerative Disorders
|
0.100 |
Biomarker
|
group |
BEFREE |
Reduced expression of the survival motor neuron (SMN) protein causes the neurodegenerative disease spinal muscular atrophy (SMA).
|
31851921 |
2019 |
|
Spinal Muscular Atrophy
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
ZPR1 overexpression in vivo results in a systemic increase of SMN levels and rescues severe to moderate disease in SMA mice.
|
31828288 |
2020 |
|
Spinal Muscular Atrophy
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The combined treatment of SMA cells with sub-optimal doses of LBH589 and of an antisense oligonucleotide that mimic Nusinersen (ASO_ISSN1) elicits additive effects on SMN2 splicing and SMN protein expression.
|
31811660 |
2019 |
|
Motor Neuron Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Spinal muscular atrophy (SMA) is a motor neuron disease caused by loss of function mutations in the Survival Motor Neuron 1 (SMN1) gene and reduced expression of the SMN protein, leading to spinal motor neuron death, muscle weakness and atrophy.
|
31811660 |
2019 |
|
Neoplasm Metastasis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Stathmin mediates cell migration and invasion in vitro, and metastasis in vivo.
|
31806880 |
2020 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Our findings demonstrate that stathmin levels can regulate PTPN14 expression, which can modulate neuroblastoma cell migration and invasion.
|
31806880 |
2020 |
|
Neuroblastoma
|
0.060 |
AlteredExpression
|
disease |
BEFREE |
Consistent with gene array data, PTPN14 mRNA and protein expression were downregulated in stathmin- depleted neuroblastoma cells and xenografts.
|
31806880 |
2020 |
|
Central neuroblastoma
|
0.060 |
AlteredExpression
|
disease |
BEFREE |
Consistent with gene array data, PTPN14 mRNA and protein expression were downregulated in stathmin- depleted neuroblastoma cells and xenografts.
|
31806880 |
2020 |
|
Childhood Neuroblastoma
|
0.060 |
AlteredExpression
|
disease |
BEFREE |
Consistent with gene array data, PTPN14 mRNA and protein expression were downregulated in stathmin- depleted neuroblastoma cells and xenografts.
|
31806880 |
2020 |
|
Spinal Muscular Atrophy
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In this study, we investigated the disease modifying potential of reduced EphA4 protein levels in the SMNΔ7 mouse model for severe SMA.
|
31803009 |
2019 |
|
Spinal Muscular Atrophy
|
0.100 |
Biomarker
|
disease |
BEFREE |
SMN deficiency causes neurodegenerative disease spinal muscular atrophy (SMA).
|
31799625 |
2020 |
|
Neurodegenerative Disorders
|
0.100 |
Biomarker
|
group |
BEFREE |
SMN deficiency causes neurodegenerative disease spinal muscular atrophy (SMA).
|
31799625 |
2020 |
|
Spinal Muscular Atrophy
|
0.100 |
Biomarker
|
disease |
BEFREE |
This is an orthologue of the stasimon/tmem41b gene, a downstream target of SMN, the depleted protein in spinal muscular atrophy (SMA), which partially recapitulates the SMA phenotype in fly and zebrafish models when mutated.
|
31797327 |
2020 |
|
Liver carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Further experiments demonstrated that STMN1 mediated intricate crosstalk between HCCs and hepatic stellate cells (HSCs) via triggering the HGF/MET signal pathway.
|
31785057 |
2020 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
STMN1 upregulation mediates HCC and hepatic stellate cells crosstalk to aggravate cancer through triggering MET pathway.
|
31785057 |
2020 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
STMN1 upregulation mediates HCC and hepatic stellate cells crosstalk to aggravate cancer through triggering MET pathway.
|
31785057 |
2020 |
|
Liver carcinoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Finally, murine and human HCC data indicate significant correlations of STMN1 expression with E2F1/TFPD1 and with KPNA2 expression and their association with poor prognosis in HCC patients.
|
31783876 |
2019 |
|
Adult Liver Carcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Karyopherin α2-dependent import of E2F1 and TFDP1 maintains protumorigenic stathmin expression in liver cancer.
|
31783876 |
2019 |
|
Liver and Intrahepatic Biliary Tract Carcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Karyopherin α2-dependent import of E2F1 and TFDP1 maintains protumorigenic stathmin expression in liver cancer.
|
31783876 |
2019 |
|
Malignant neoplasm of liver
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Karyopherin α2-dependent import of E2F1 and TFDP1 maintains protumorigenic stathmin expression in liver cancer.
|
31783876 |
2019 |
|
Spinal Muscular Atrophy
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
<b>Background:</b> 5q spinal muscular atrophy (SMA) is an autosomal recessive lower motoneuron disease caused by deletion or mutations in the survival motor neuron 1 gene (<i>SMN1</i>) which results in reduced expression of full-length SMN protein.
|
31736847 |
2019 |
|
Inverted Papilloma
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Dysplasia was present in 26,7% of IPs with high stathmin expression while only 7.4% of IPs with low stathmin expression showed dysplasia.
|
31710049 |
2020 |
|
Inverted Squamous Cell Papilloma
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Dysplasia was present in 26,7% of IPs with high stathmin expression while only 7.4% of IPs with low stathmin expression showed dysplasia.
|
31710049 |
2020 |
|
Primary peritoneal carcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Here, we clarified the prognostic impact of these drug-sensitivity markers in PPC by performing immunohistochemical and clinicopathologic analyses of samples from 105 patients with surgically resected PPC in order to evaluate levels of vascular endothelial growth factor 2 (VEGFR2), stathmin 1 (STMN1), tubulin β3 class III (TUBB3), thymidylate synthetase (TS), topoisomerase II (Topo-II), glucose-regulated protein, and 78 kDa (GRP78)/binding immunoglobulin protein (BiP).
|
31653009 |
2019 |