|
Reperfusion Injury
|
0.200 |
Biomarker
|
disease |
RGD |
Role of perfusion medium, oxygen and rheology for endoplasmic reticulum stress-induced cell death after hypothermic machine preservation of the liver.
|
18005084 |
2008 |
|
Invasive Ductal Breast Carcinoma
|
0.200 |
ModifyingMutation
|
disease |
RGD |
Identification of transmembrane proteins as potential prognostic markers and therapeutic targets in breast cancer by a screen for signal sequence encoding transcripts.
|
17054309 |
2006 |
|
Ductal Breast Carcinoma
|
0.200 |
ModifyingMutation
|
disease |
RGD |
Identification of transmembrane proteins as potential prognostic markers and therapeutic targets in breast cancer by a screen for signal sequence encoding transcripts.
|
17054309 |
2006 |
|
Systolic Pressure
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Intelligence
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function.
|
29844566 |
2018 |
|
Malignant Neoplasms
|
0.050 |
AlteredExpression
|
group |
BEFREE |
Altogether, this study suggests the involvement of Sp1 in basal transcription and PKC in the enhanced expression of TMBIM6 in cancer.
|
31336725 |
2019 |
|
Neoplasm Metastasis
|
0.050 |
AlteredExpression
|
phenotype |
BEFREE |
While most studies have demonstrated a beneficial role for BI-1 in the ubiquitous maintenance of cellular homeostasis, its expression in cancer cells seems most often to contribute to tumorigenesis and metastasis.
|
31841271 |
2019 |
|
Neoplasm Metastasis
|
0.050 |
AlteredExpression
|
phenotype |
BEFREE |
Transmembrane Bax Inhibitor Motif-containing 6 (TMBIM6) is upregulated in several cancer types and involved in the metastasis.
|
31336725 |
2019 |
|
Carcinogenesis
|
0.050 |
AlteredExpression
|
phenotype |
BEFREE |
While most studies have demonstrated a beneficial role for BI-1 in the ubiquitous maintenance of cellular homeostasis, its expression in cancer cells seems most often to contribute to tumorigenesis and metastasis.
|
31841271 |
2019 |
|
Malignant Neoplasms
|
0.050 |
Biomarker
|
group |
BEFREE |
However, BI-1 is also a negative regulator of the endoplasmic reticulum stress sensor IRE1 α, it interacts with G-actin and increases actin polymerization, enhances cancer metastasis by altering glucose metabolism and activating the sodium-hydrogen exchanger, and reduces the production of reactive oxygen species through direct interaction with NADPH-P450 reductase.
|
21663964 |
2011 |
|
Neoplasm Metastasis
|
0.050 |
Biomarker
|
phenotype |
BEFREE |
However, BI-1 is also a negative regulator of the endoplasmic reticulum stress sensor IRE1 α, it interacts with G-actin and increases actin polymerization, enhances cancer metastasis by altering glucose metabolism and activating the sodium-hydrogen exchanger, and reduces the production of reactive oxygen species through direct interaction with NADPH-P450 reductase.
|
21663964 |
2011 |
|
Carcinogenesis
|
0.050 |
Biomarker
|
phenotype |
BEFREE |
Taken together, these data lead us to conclude that Bi-1 plays a crucial role in CNE-1 tumorigenesis and that Bi-1 may be a novel therapeutic target for nasopharyngeal carcinoma.
|
21545297 |
2011 |
|
Malignant Neoplasms
|
0.050 |
GeneticVariation
|
group |
BEFREE |
In both in vitro and in vivo experiments, C-terminal deleted (CDeltaBI-1) cells showed similar results to control cells, suggesting that the C-terminal motif is required for BI-1-associated alterations of glucose metabolism, NHE activation and cancer metastasis.
|
20118983 |
2010 |
|
Neoplasm Metastasis
|
0.050 |
Biomarker
|
phenotype |
BEFREE |
These findings strongly suggest that BI-1 reduces extracellular pH and regulates metastasis by altering glucose metabolism and activating NHE, with the C-terminal tail having a pivotal role in these processes.
|
20118983 |
2010 |
|
Carcinogenesis
|
0.050 |
Biomarker
|
phenotype |
BEFREE |
To investigate the potential role of BI-1 in promoting cell growth and tumorigenesis, in the present study we overexpressed the BI-1 gene in NIH3T3 cells using the lentivirus-mediated gene expression system.
|
20597862 |
2010 |
|
Carcinogenesis
|
0.050 |
AlteredExpression
|
phenotype |
BEFREE |
The high BI-1 mRNAs levels observed in early liver disease may protect virus-infected cells against apoptosis, while their progressive downregulation may facilitate hepatocellular carcinogenesis.
|
20359348 |
2010 |
|
Malignant Neoplasms
|
0.050 |
AlteredExpression
|
group |
BEFREE |
As BI-1 is (over-) expressed in a broad variety of malignancies, it may represent an interesting novel TAA in the context of cancer vaccines.
|
19609282 |
2009 |
|
Carcinogenesis
|
0.050 |
Biomarker
|
phenotype |
BEFREE |
The Bax Inhibitor-1 (BI-1) family in apoptosis and tumorigenesis.
|
18336295 |
2008 |
|
Malignant Neoplasms
|
0.050 |
AlteredExpression
|
group |
BEFREE |
Furthermore, BI-1 expression analysis using a cancer profiling array showed up-regulation of BI-1 expression in cancer samples of breast, uterus and ovary, whereas down-regulated BI-1 expression was identified in stomach, colon, kidney, lung and rectal cancer.
|
16353131 |
2006 |
|
Neoplasm Metastasis
|
0.050 |
AlteredExpression
|
phenotype |
BEFREE |
Some of these genes were already known to be associated with apoptosis (BIK, TEGT, SSI-3), hypoxia-inducible genes (HIF1A, CA12), and tumor cell invasion and metastasis (CTSL, CTSB, PLAU, CD44).
|
15337562 |
2004 |
|
Primary malignant neoplasm
|
0.040 |
AlteredExpression
|
group |
BEFREE |
Altogether, this study suggests the involvement of Sp1 in basal transcription and PKC in the enhanced expression of TMBIM6 in cancer.
|
31336725 |
2019 |
|
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
Among the 182 genes, nine candidates (CHCHD1, GNB2L1, IPO8, LASP1, RPL27A, RPS12, SOD1, SRSF9, TMBIM6) that were not associated with tumor volume, stage, lymph node involvement or disease progression in array data of 150 patients, were selected for further testing by RT-qPCR. geNorm and NormFinder analyses of RT-qPCR data of 74 patients identified CHCHD1, SRSF9 and TMBIM6 as the optimal set of reference genes, with stable expression both overall and across patient subgroups with different hypoxia status (ABrix) and clinical parameters.
|
27244197 |
2016 |
|
Neoplasms
|
0.040 |
AlteredExpression
|
group |
BEFREE |
Furthermore, BI-1-deficient mice show reduced basal autophagy, and experimentally reducing BI-1 expression impairs tumor xenograft growth in vivo.
|
22588718 |
2012 |
|
Primary malignant neoplasm
|
0.040 |
Biomarker
|
group |
BEFREE |
However, BI-1 is also a negative regulator of the endoplasmic reticulum stress sensor IRE1 α, it interacts with G-actin and increases actin polymerization, enhances cancer metastasis by altering glucose metabolism and activating the sodium-hydrogen exchanger, and reduces the production of reactive oxygen species through direct interaction with NADPH-P450 reductase.
|
21663964 |
2011 |
|
Primary malignant neoplasm
|
0.040 |
GeneticVariation
|
group |
BEFREE |
In both in vitro and in vivo experiments, C-terminal deleted (CDeltaBI-1) cells showed similar results to control cells, suggesting that the C-terminal motif is required for BI-1-associated alterations of glucose metabolism, NHE activation and cancer metastasis.
|
20118983 |
2010 |