Malignant Neoplasms
|
0.050 |
Biomarker
|
group |
BEFREE |
Thus, CSL inhibition may provide a more effective mechanism to inhibit Notch-pathway dependent cancer cell proliferation as compared to GSI treatment.
|
21520243 |
2011 |
Malignant Neoplasms
|
0.050 |
AlteredExpression
|
group |
BEFREE |
Thus, ATF3 converges with CSL in negative control of CAF activation with epigenetic changes amenable to cancer- and stroma-focused intervention.
|
28684431 |
2017 |
Malignant Neoplasms
|
0.050 |
Biomarker
|
group |
BEFREE |
Taken together, the findings point to a central role of CSL in telomere homeostasis with important implications for genomic instability of cancer stromal cells and beyond.
|
31467287 |
2019 |
Malignant Neoplasms
|
0.050 |
Biomarker
|
group |
BEFREE |
CSL, the key effector of canonical Notch signaling endowed with an intrinsic transcription repressive function, suppresses stromal fibroblast senescence and Cancer Associated Fibroblast (CAF) activation through direct down-modulation of key effector genes.
|
27542230 |
2016 |
Malignant Neoplasms
|
0.050 |
AlteredExpression
|
group |
BEFREE |
Combined CSL and p53 downregulation promotes cancer-associated fibroblast activation.
|
26302407 |
2015 |
Primary malignant neoplasm
|
0.050 |
Biomarker
|
group |
BEFREE |
Taken together, the findings point to a central role of CSL in telomere homeostasis with important implications for genomic instability of cancer stromal cells and beyond.
|
31467287 |
2019 |
Primary malignant neoplasm
|
0.050 |
Biomarker
|
group |
BEFREE |
CSL, the key effector of canonical Notch signaling endowed with an intrinsic transcription repressive function, suppresses stromal fibroblast senescence and Cancer Associated Fibroblast (CAF) activation through direct down-modulation of key effector genes.
|
27542230 |
2016 |
Primary malignant neoplasm
|
0.050 |
AlteredExpression
|
group |
BEFREE |
Combined CSL and p53 downregulation promotes cancer-associated fibroblast activation.
|
26302407 |
2015 |
Primary malignant neoplasm
|
0.050 |
AlteredExpression
|
group |
BEFREE |
Thus, ATF3 converges with CSL in negative control of CAF activation with epigenetic changes amenable to cancer- and stroma-focused intervention.
|
28684431 |
2017 |
Primary malignant neoplasm
|
0.050 |
Biomarker
|
group |
BEFREE |
Thus, CSL inhibition may provide a more effective mechanism to inhibit Notch-pathway dependent cancer cell proliferation as compared to GSI treatment.
|
21520243 |
2011 |
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
All canonical Notch signaling is transmitted through the DNA-binding protein CSL, and hyperactivated Notch signaling is associated with tumor development; thus it may be anticipated that CSL deficiency should reduce tumor growth.
|
27066863 |
2016 |
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
In vivo, SCC cells with increased CSL levels gave rise to rapidly expanding tumors, while cells with silenced CSL formed smaller and more differentiated tumors with enhanced inflammatory infiltrate.
|
29757189 |
2018 |
Neoplasms
|
0.040 |
AlteredExpression
|
group |
BEFREE |
We report that, in human dermal fibroblasts (HDFs), conditions inducing autophagy-often found in tumor stroma-down-regulate CSL protein levels but do not affect its mRNA levels.
|
30231994 |
2018 |
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
CSL-deficient dermal fibroblasts promote increased tumor cell proliferation through upregulation of c-Jun and c-Fos expression and consequently higher levels of diffusible growth factors, inflammatory cytokines, and matrix-remodeling enzymes.
|
22682244 |
2012 |
Precancerous Conditions
|
0.010 |
Biomarker
|
group |
BEFREE |
CSL is downmodulated in stromal fibroblasts of premalignant skin actinic keratosis lesions and squamous cell carcinomas, whereas p53 expression and function are downmodulated only in the latter, with paracrine FGF signalling as the probable culprit.
|
26302407 |
2015 |
Mammary Neoplasms
|
0.010 |
AlteredExpression
|
group |
BEFREE |
Down-regulation of CSL also suppressed the proliferation of ErbB2-negative breast tumor cell lines, indicating that the NOTCH-CSL signaling axis is involved in cell proliferation.
|
18339869 |
2008 |
hearing impairment
|
0.330 |
Biomarker
|
phenotype |
GENOMICS_ENGLAND |
A novel locus for non-syndromic sensorineural deafness (DFN6) maps to chromosome Xp22.
|
8872482 |
1996 |
hearing impairment
|
0.330 |
GeneticVariation
|
phenotype |
BEFREE |
Collectively, this study is the first to report the role of SMPX in Chinese population and identify a novel frameshift mutation in SMPX that causes not only nonsyndromic late-onset progressive HL, but also congenital hearing impairment.
|
28542515 |
2017 |
hearing impairment
|
0.330 |
Biomarker
|
phenotype |
BEFREE |
Variable degrees of hearing impairment in a Dutch DFNX4 (DFN6) family.
|
21893181 |
2011 |
hearing impairment
|
0.330 |
AlteredExpression
|
phenotype |
BEFREE |
SMPX had previously been demonstrated to be specifically expressed in striated muscle and, therefore, seemed an unlikely candidate gene for hearing impairment.
|
21549342 |
2011 |
Childhood onset
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
X-linked dominant inheritance
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
Carcinogenesis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
Collectively, this suggests that CSL exerts functions beyond serving as the central node in the Notch signaling cascade and reveals a role for CSL in tumorigenesis and regulation of the cellular hypoxic response.
|
27066863 |
2016 |
Carcinogenesis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
The Notch/CSL pathway plays an important role in skin homeostasis and carcinogenesis.
|
27542230 |
2016 |
Carcinogenesis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
The Notch signaling pathway transcriptional regulator, CSL (also called as CBF1, Suppressor of Hairless or Lag-1 in different species, generally designated as CSL1), is not only associated with cell proliferation and differentiation but also involved in tumorigenesis, inflammation and immune regulation in vertebrates.
|
30031869 |
2018 |