INT256746

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Context Info
Confidence 0.16
First Reported 2009
Last Reported 2010
Negated 3
Speculated 0
Reported most in Body
Documents 17
Total Number 18
Disease Relevance 4.18
Pain Relevance 0.42

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Cdr1 (Mus musculus)
Pain Link Frequency Relevance Heat
cva 118 99.22 Very High Very High Very High
imagery 2 10.56 Low Low
Pain 16 5.00 Very Low Very Low Very Low
Angina 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Attention Deficit Hyperactivity Disorder 64 99.32 Very High Very High Very High
Pulmonary Embolism 110 99.22 Very High Very High Very High
Sprains And Strains 896 99.12 Very High Very High Very High
Fungal Infection 96 86.08 High High
Parkinson's Disease 48 85.12 High High
Infection 224 61.56 Quite High
Embolism 10 60.60 Quite High
Invasive Candidiasis 16 56.04 Quite High
Reprotox - General 1 16 53.16 Quite High
Disease 64 32.80 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However the failure rate of 2.7% is exceeded in both qualitative POC D-dimer tests when combined with a Wells-CDR cut off value of ?
Gene_expression (cut) of CDR
1) Confidence 0.16 Published 2010 Journal BMC Fam Pract Section Body Doc Link PMC2944151 Disease Relevance 0.42 Pain Relevance 0.18
In the Christopher-study PE could be excluded safely with a Wells-CDR cut-off value of ?
Gene_expression (cut) of CDR associated with cva
2) Confidence 0.14 Published 2010 Journal BMC Fam Pract Section Body Doc Link PMC2944151 Disease Relevance 0.55 Pain Relevance 0.24
Interestingly, the P822L substitution is responsible for the constitutive overexpression of CgSNQ2, but has no effect on the expression of CgCDR1 and CgCDR2 [17].
Gene_expression (expression) of CgCDR1
3) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.39 Pain Relevance 0
Single point mutations in CgPDR1 have been shown to increase the expression of both CgCDR genes and CgPDR1, thus contributing to azole resistance of clinical isolates [14],[15].
Gene_expression (expression) of CgCDR
4) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.13 Pain Relevance 0
Two studies have identified three separate amino acid substitutions (W297S, F575L, P927L) in CgPdr1p of azole-resistant strains that are responsible for constitutive high expression of CgCDR1, CgCDR2 and CgPDR1 itself [14],[15].
Gene_expression (expression) of CgCDR1 associated with sprains and strains
5) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.31 Pain Relevance 0
Expression of the CgCDR1, CgCDR2 and CgSNQ2 genes was quantitatively assessed with real-time RT-PCR in an i-Cycler iQ system (Bio-Rad).
Gene_expression (Expression) of CgCDR1
6) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.10 Pain Relevance 0
In C. glabrata, the constitutive upregulated expression of ABC-transporter genes CgCDR1 and, to a lesser extent, CgCDR2 (also known as PDH1) plays a dominant role in azole resistance [4], [8]–[11].
Gene_expression (expression) of CgCDR1
7) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.34 Pain Relevance 0
Single-point mutations in CgPDR1 are known to increase the expression of at least CgCDR1 and CgCDR2 and thus to contribute to azole resistance of clinical isolates.
Gene_expression (expression) of CgCDR1
8) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Abstract Doc Link PMC2607542 Disease Relevance 0.13 Pain Relevance 0
Since only alleles containing these mutations conferred CgCDR1 constitutive high expression (from 4- to 150-fold expression increase, Figure 6B), these mutations could be assigned as GOF mutations.
Gene_expression (expression) of CgCDR1
9) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.28 Pain Relevance 0
As previously observed by Torelli et al. [17], CgCDR1, CgCDR2 and CgSNQ2 were not always coordinately expressed in azole-resistant isolates.
Neg (not) Gene_expression (expressed) of CgCDR1
10) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.16 Pain Relevance 0
The expression of CgCDR genes is regulated by a single Zn(2)-Cys(6) transcription factor, CgPdr1p, an homologue of S. cerevisiae Pdr1p/Pdr3p [11].
Gene_expression (expression) of CgCDR
11) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.14 Pain Relevance 0
Expression of the CgPDR1 allele containing the L280F substitution was sufficient to confer CgCdr1p and CgCdr2p constitutive high expression and thus azole resistance in C. glabrata independently on the strain genetic background (Figure 5C).
Gene_expression (expression) of CgCdr1p associated with sprains and strains
12) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.32 Pain Relevance 0
Surprisingly, our results show that CgCDR1, CgCDR2 and CgSNQ2 are not coordinately expressed in azole-resistant isolates.
Neg (not) Gene_expression (expressed) of CgCDR1
13) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.08 Pain Relevance 0
Interestingly, the major transporters involved in azole resistance (CgCDR1, CgCDR2, and CgSNQ2) were not always coordinately expressed in presence of specific CgPDR1 GOF mutations, thus suggesting that these are rather trans-acting elements (GOF in CgPDR1) than cis-acting elements (promoters) that lead to azole resistance by upregulating specific combinations of ABC-transporter genes.
Neg (not) Gene_expression (expressed) of CgCDR1
14) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Abstract Doc Link PMC2607542 Disease Relevance 0.17 Pain Relevance 0
We hypothesized that CgPDR1 mutations may confer enhanced activity (or hyperactivity) to CgPdr1p leading to increased expression of the CgCDR and/or CgSNQ2 genes.
Gene_expression (expression) of CgCDR associated with attention deficit hyperactivity disorder
15) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.18 Pain Relevance 0
Four single amino acid substitutions in CgPdr1p (W297S, F575L, P822L and P927L) have been reported to increase the expression of at least CgCDR1, CgCDR2 and CgSNQ2 and thus to contribute to azole resistance of clinical isolates [14],[15].
Gene_expression (expression) of CgCDR1
16) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0 Pain Relevance 0
Expression of CgCDR1, CgCDR2 and CgSNQ2 in reconstituted strains was restored to similar levels than those of the original clinical isolates (Figure 5B).
Gene_expression (Expression) of CgCDR1 associated with sprains and strains
17) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.32 Pain Relevance 0
For example, the presence of the Y584C substitution (from CgPDR1 of DSY754) led to CgCDR1 upregulation only (17- and 12-fold expression increase, Figure 1 and Figure 6B), whereas the presence of the T588A substitution (from CgPDR1 of DSY2234) resulted in high mRNA levels of both CgCDR genes (4- and 8-fold expression increase for CgCDR1, 23- and 30-fold increase for CgCDR2, Figure 1 and Figure 6B).
Gene_expression (expression) of CgCDR1
18) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2607542 Disease Relevance 0.16 Pain Relevance 0

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