|
Osteosarcoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In this report, we show that when human osteosarcoma derived clonal cells (TE 85 clone F-5) (HOS), which are immortalized and nontumorigenic, undergo transformation following infection by Kirsten murine sarcoma virus (K-HOS) or by a chemical carcinogen [N-methyl-N-nitro-N-nitrosoguanidine (MNNG-HOS)], the smooth muscle MLC-2 mRNA is repressed.
|
1599878 |
1992 |
|
Osteosarcoma of bone
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In this report, we show that when human osteosarcoma derived clonal cells (TE 85 clone F-5) (HOS), which are immortalized and nontumorigenic, undergo transformation following infection by Kirsten murine sarcoma virus (K-HOS) or by a chemical carcinogen [N-methyl-N-nitro-N-nitrosoguanidine (MNNG-HOS)], the smooth muscle MLC-2 mRNA is repressed.
|
1599878 |
1992 |
|
Sarcoma
|
0.010 |
AlteredExpression
|
group |
BEFREE |
In this report, we show that when human osteosarcoma derived clonal cells (TE 85 clone F-5) (HOS), which are immortalized and nontumorigenic, undergo transformation following infection by Kirsten murine sarcoma virus (K-HOS) or by a chemical carcinogen [N-methyl-N-nitro-N-nitrosoguanidine (MNNG-HOS)], the smooth muscle MLC-2 mRNA is repressed.
|
1599878 |
1992 |
|
Childhood Osteosarcoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In this report, we show that when human osteosarcoma derived clonal cells (TE 85 clone F-5) (HOS), which are immortalized and nontumorigenic, undergo transformation following infection by Kirsten murine sarcoma virus (K-HOS) or by a chemical carcinogen [N-methyl-N-nitro-N-nitrosoguanidine (MNNG-HOS)], the smooth muscle MLC-2 mRNA is repressed.
|
1599878 |
1992 |
|
Malignant neoplasm of soft tissue
|
0.010 |
AlteredExpression
|
group |
BEFREE |
In this report, we show that when human osteosarcoma derived clonal cells (TE 85 clone F-5) (HOS), which are immortalized and nontumorigenic, undergo transformation following infection by Kirsten murine sarcoma virus (K-HOS) or by a chemical carcinogen [N-methyl-N-nitro-N-nitrosoguanidine (MNNG-HOS)], the smooth muscle MLC-2 mRNA is repressed.
|
1599878 |
1992 |
|
Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
The significance for pVHL function of two further genes upregulated by wild-type pVHL was initially unclear, but re-expression of GNG4 (G protein gamma-4 subunit/guanine nucleotide-binding protein-4) and MLC2 (myosin light chain) in a RCC cell line suppressed tumour cell growth. pVHL regulation of CDKN1C, SPARC and GNG4 was not mimicked by hypoxia, whereas for six of 11 novel targets analysed (including DOC-2/DAB2 and MLC2) the effects of pVHL inactivation and hypoxia were similar.
|
15824735 |
2005 |
|
Cardiomyopathy, Hypertrophic, Familial
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
The E22K mutation of myosin RLC that causes familial hypertrophic cardiomyopathy increases calcium sensitivity of force and ATPase in transgenic mice.
|
16076902 |
2005 |
|
Renal Cell Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
The significance for pVHL function of two further genes upregulated by wild-type pVHL was initially unclear, but re-expression of GNG4 (G protein gamma-4 subunit/guanine nucleotide-binding protein-4) and MLC2 (myosin light chain) in a RCC cell line suppressed tumour cell growth. pVHL regulation of CDKN1C, SPARC and GNG4 was not mimicked by hypoxia, whereas for six of 11 novel targets analysed (including DOC-2/DAB2 and MLC2) the effects of pVHL inactivation and hypoxia were similar.
|
15824735 |
2005 |
|
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
The significance for pVHL function of two further genes upregulated by wild-type pVHL was initially unclear, but re-expression of GNG4 (G protein gamma-4 subunit/guanine nucleotide-binding protein-4) and MLC2 (myosin light chain) in a RCC cell line suppressed tumour cell growth. pVHL regulation of CDKN1C, SPARC and GNG4 was not mimicked by hypoxia, whereas for six of 11 novel targets analysed (including DOC-2/DAB2 and MLC2) the effects of pVHL inactivation and hypoxia were similar.
|
15824735 |
2005 |
|
Hyperlipoproteinemia Type IIa
|
0.020 |
Biomarker
|
disease |
BEFREE |
Prolonged Ca2+ and force transients in myosin RLC transgenic mouse fibers expressing malignant and benign FHC mutations.
|
16837010 |
2006 |
|
Cerebral Edema
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Inhibition of the myosin light chain kinase prevents hypoxia-induced blood-brain barrier disruption.
|
17419808 |
2007 |
|
Vasogenic Cerebral Edema
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Inhibition of the myosin light chain kinase prevents hypoxia-induced blood-brain barrier disruption.
|
17419808 |
2007 |
|
Cytotoxic Cerebral Edema
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Inhibition of the myosin light chain kinase prevents hypoxia-induced blood-brain barrier disruption.
|
17419808 |
2007 |
|
Vasogenic Brain Edema
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Inhibition of the myosin light chain kinase prevents hypoxia-induced blood-brain barrier disruption.
|
17419808 |
2007 |
|
Cytotoxic Brain Edema
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Inhibition of the myosin light chain kinase prevents hypoxia-induced blood-brain barrier disruption.
|
17419808 |
2007 |
|
Brain Edema
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Inhibition of the myosin light chain kinase prevents hypoxia-induced blood-brain barrier disruption.
|
17419808 |
2007 |
|
Vascular Diseases
|
0.300 |
Biomarker
|
group |
CTD_human |
Regulation of myosin light chain kinase expression by angiotensin II in hypertension.
|
18511912 |
2008 |
|
Tumor Cell Invasion
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
Two of these, MYH9 (NMHCIIa) and MYL9 (MLC2), are also required for invasion and lung colonization.
|
19198601 |
2009 |
|
Glomerulonephritis
|
0.010 |
Biomarker
|
disease |
BEFREE |
In the kidney and immune organs, only Ifi202 expression increased with the development of GN in B6.MRLc1(82-100), and significant differences from C57BL/6 were observed even before disease onset.
|
20167632 |
2010 |
|
Thrombocytopenia
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Regulation of platelet myosin light chain (MYL9) by RUNX1: implications for thrombocytopenia and platelet dysfunction in RUNX1 haplodeficiency.
|
20876458 |
2010 |
|
Endometriosis
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Three proteins, collapsin response mediator protein 2 (CRMP2), ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCH-L1) and myosin regulatory light polypeptide 9 (MYL9), were simultaneously identified from the two sets of samples from females with or without endometriosis by two-dimensional electrophoresis (2-DE).
|
23670619 |
2013 |
|
Liver Cirrhosis, Experimental
|
0.300 |
Biomarker
|
disease |
CTD_human |
Systems level analysis and identification of pathways and networks associated with liver fibrosis.
|
25380136 |
2014 |
|
Neoplasm Metastasis
|
0.030 |
AlteredExpression
|
phenotype |
BEFREE |
In addition, MYL9 was mainly expressed in the cytoplasm of stromal cells of prostate tissues, and the decreased expression of MYL9 in PCa tissues was significantly correlated with the older age of patients (P = 0.011), the higher Gleason score (P < 0.001), the advanced pathological stage (P = 0.002), the presence of metastasis (P < 0.001) and PSA failure (P = 0.001).
|
24338276 |
2014 |
|
Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
And then, the expression levels of two selected genes in the down-regulated co-pathways, myosin light chain kinase (MYLK) and myosin regulatory light chain 9 (MYL9), were determined in tumor, paired paraneoplastic, and normal lung tissues.
|
25179839 |
2014 |
|
Cardiomyopathy, Hypertrophic, Familial
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
This study focuses on the aspartic acid to valine substitution (D166V) in the myosin RLC shown to be associated with a malignant phenotype of familial hypertrophic cardiomyopathy (FHC).
|
24374283 |
2014 |