INT278810

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Context Info
Confidence 0.32
First Reported 2009
Last Reported 2009
Negated 0
Speculated 1
Reported most in Body
Documents 1
Total Number 15
Disease Relevance 0.64
Pain Relevance 0

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

nucleus (HOXA9) cytoplasm (HOXA9)
Anatomy Link Frequency
terminal portion 1
HOXA9 (Homo sapiens)
HOXA9 - N51S (2)
Pain Link Frequency Relevance Heat
cytokine 30 35.84 Quite Low
cINOD 45 11.48 Low Low
aspirin 30 5.96 Low Low
Disease Link Frequency Relevance Heat
Leukemia 120 96.96 Very High Very High Very High
Cancer 105 75.36 Quite High
Myeloid Leukemia 90 60.40 Quite High
Chronic Lymphoid Leukemia 30 54.60 Quite High
Hematologic Neoplasms 30 53.04 Quite High
Cytomegalovirus Infection 45 39.68 Quite Low
Lymphatic System Cancer 30 10.24 Low Low
INFLAMMATION 15 7.64 Low Low
Repression 15 5.00 Very Low Very Low Very Low
Adhesions 15 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The fold change of each probe set was calculated by dividing the absolute signal intensity from NUP98-HOXA9, NUP98-HOXA9/N51S, HOXA9, and HOXA9?
HOXA9 (N51S) Binding (intensity) of
1) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0.08 Pain Relevance 0
The data suggest that the effect of NUP98-HOXA9 on cell numbers is partially dependent on classical transactivation involving DNA binding and partially on mechanisms other than DNA binding.
HOXA9 Spec (partially) Binding (binding) of
2) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0 Pain Relevance 0
The data suggest that the effect of NUP98-HOXA9 on cell numbers is partially dependent on classical transactivation involving DNA binding and partially on mechanisms other than DNA binding.
HOXA9 Binding (binding) of
3) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0 Pain Relevance 0
The fold change of each probe set was calculated by dividing the absolute signal intensity from NUP98-HOXA9, NUP98-HOXA9/N51S, HOXA9, and HOXA9?
HOXA9 Binding (intensity) of
4) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0.08 Pain Relevance 0
Therefore it is unlikely to represent direct specific binding of the homeodomain to the promoter, but it could represent a very weak indirect interaction between NUP98-HOXA9 and the PLN promoter that is difficult to detect by our ChIP assays.
HOXA9 Binding (interaction) of
5) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0 Pain Relevance 0
The fold change of each probe set was calculated by dividing the absolute signal intensity from NUP98-HOXA9, NUP98-HOXA9/N51S, HOXA9, and HOXA9?
HOXA9 Binding (intensity) of
6) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0.08 Pain Relevance 0
NUP98-HOXA9 showed association with the KBTBD10 promoter whereas NUP98-HOXA9/N51S did not show significant binding (Fig. 5B).
HOXA9 Binding (association) of
7) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0 Pain Relevance 0
NUP98-HOXA9 showed association with the KBTBD10 promoter whereas NUP98-HOXA9/N51S did not show significant binding (Fig. 5B).
HOXA9 Binding (binding) of
8) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0 Pain Relevance 0
The ability of NUP98-HOXA9/N51S to recapitulate most of the effects of NUP98-HOXA9 suggests that the disruption of hematopoietic differentiation by NUP98-HOXA9 is largely attributable to the NUP98 moiety and does not require DNA binding by the homeodomain.
HOXA9 Binding (binding) of
9) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0 Pain Relevance 0
There may be very weak binding of NUP98-HOXA9 to the segment amplified by the PLN (3) primer set.
HOXA9 Binding (binding) of
10) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0 Pain Relevance 0
The luciferase reporter and ChIP data in K562 cells demonstrate at least two modes by which the NUP98-HOXA9 oncogene can dysregulate gene transcription: one that correlates with DNA-binding through the HOXA9 homeodomain and another that does not.
HOXA9 Binding (binding) of
11) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0.16 Pain Relevance 0
Here we show that NUP98-HOXA9 can regulate transcription without binding to DNA.
HOXA9 Binding (binding) of
12) Confidence 0.31 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2725295 Disease Relevance 0.09 Pain Relevance 0
Future experiments directed at identifying proteins that interact with NUP98-HOXA9 and examining its effects on nucleocytoplasmic transport may elucidate the homeodomain-independent mechanisms that contribute to the leukemogenic functions of NUP98 fusion proteins.
HOXA9 Binding (interact) of
13) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0.06 Pain Relevance 0
It consists of an N-terminal portion of NUP98 fused to the homeodomain of HOXA9 and is believed to act as an aberrant transcription factor that binds DNA through the homeodomain.
HOXA9 Binding (binds) of in terminal portion
14) Confidence 0.31 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2725295 Disease Relevance 0.10 Pain Relevance 0
Neither NUP98-HOXA9 nor NUP98-HOXA9/N51S showed significant binding to the segment of the PLN promoter that is transactivated by NUP98-HOXA9 (Fig. 5B).
HOXA9 (N51S) Binding (binding) of
15) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2725295 Disease Relevance 0 Pain Relevance 0

General Comments

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