| Tchem | DNA topoisomerase 2-beta |
Control of topological states of DNA by transient breakage and subsequent rejoining of DNA strands. Topoisomerase II makes double-strand breaks.
This gene encodes a DNA topoisomerase, an enzyme that controls and alters the topologic states of DNA during transcription. This nuclear enzyme is involved in processes such as chromosome condensation, chromatid separation, and the relief of torsional stress that occurs during DNA transcription and replication. It catalyzes the transient breaking and rejoining of two strands of duplex DNA which allows the strands to pass through one another, thus altering the topology of DNA. Two forms of this enzyme exist as likely products of a gene duplication event. The gene encoding this form, beta, is localized to chromosome 3 and the alpha form is localized to chromosome 17. The gene encoding this enzyme functions as the target for several anticancer agents and a variety of mutations in this gene have been associated with the development of drug resistance. Reduced activity of this enzyme may also play a role in ataxia-telangiectasia. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Aug 2016]
This gene encodes a DNA topoisomerase, an enzyme that controls and alters the topologic states of DNA during transcription. This nuclear enzyme is involved in processes such as chromosome condensation, chromatid separation, and the relief of torsional stress that occurs during DNA transcription and replication. It catalyzes the transient breaking and rejoining of two strands of duplex DNA which allows the strands to pass through one another, thus altering the topology of DNA. Two forms of this enzyme exist as likely products of a gene duplication event. The gene encoding this form, beta, is localized to chromosome 3 and the alpha form is localized to chromosome 17. The gene encoding this enzyme functions as the target for several anticancer agents and a variety of mutations in this gene have been associated with the development of drug resistance. Reduced activity of this enzyme may also play a role in ataxia-telangiectasia. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Aug 2016]
Comments
| Disease | Target Count | Z-score | Confidence |
|---|---|---|---|
| Leukemia, Myeloid | 18 | 0.0 | 0.0 |
| Prostatic Intraepithelial Neoplasia | 11 | 0.0 | 0.0 |
| Disease | Target Count |
|---|---|
| Myeloid Leukemia | 19 |
| Prostatic Intraepithelial Neoplasias | 11 |
| Disease | Target Count | P-value |
|---|---|---|
| lung cancer | 4740 | 1.8e-04 |
| dermatomyositis | 966 | 4.6e-04 |
| Waldenstrons macroglobulinemia | 765 | 2.4e-03 |
| group 3 medulloblastoma | 4104 | 1.7e-02 |
| Disease | Target Count | Z-score | Confidence |
|---|---|---|---|
| Osteoporosis | 363 | 0.0 | 1.7 |
| Disease | log2 FC | p |
|---|---|---|
| dermatomyositis | 1.200 | 4.6e-04 |
| group 3 medulloblastoma | 1.100 | 1.7e-02 |
| lung cancer | 1.300 | 1.8e-04 |
| Waldenstrons macroglobulinemia | 1.858 | 2.4e-03 |
| Species | Source | Disease |
|---|---|---|
| Inparanoid OMA EggNOG | ||
| Inparanoid OMA EggNOG | ||
| OMA EggNOG | ||
| Inparanoid OMA EggNOG | ||
| OMA EggNOG | ||
| Inparanoid OMA EggNOG | ||
| Inparanoid OMA EggNOG | ||
| Inparanoid OMA EggNOG | ||
| Inparanoid OMA | ||
| OMA EggNOG | ||
| Inparanoid OMA EggNOG | ||
| Inparanoid OMA | ||
| Inparanoid OMA EggNOG | ||
| Inparanoid OMA EggNOG | ||
| Inparanoid OMA EggNOG | ||
| Inparanoid OMA |
MAKSGGCGAGAGVGGGNGALTWVTLFDQNNAAKKEESETANKNDSSKKLSVERVYQKKTQLEHILLRPDT 1 - 70 YIGSVEPLTQFMWVYDEDVGMNCREVTFVPGLYKIFDEILVNAADNKQRDKNMTCIKVSIDPESNIISIW 71 - 140 NNGKGIPVVEHKVEKVYVPALIFGQLLTSSNYDDDEKKVTGGRNGYGAKLCNIFSTKFTVETACKEYKHS 141 - 210 FKQTWMNNMMKTSEAKIKHFDGEDYTCITFQPDLSKFKMEKLDKDIVALMTRRAYDLAGSCRGVKVMFNG 211 - 280 KKLPVNGFRSYVDLYVKDKLDETGVALKVIHELANERWDVCLTLSEKGFQQISFVNSIATTKGGRHVDYV 281 - 350 VDQVVGKLIEVVKKKNKAGVSVKPFQVKNHIWVFINCLIENPTFDSQTKENMTLQPKSFGSKCQLSEKFF 351 - 420 KAASNCGIVESILNWVKFKAQTQLNKKCSSVKYSKIKGIPKLDDANDAGGKHSLECTLILTEGDSAKSLA 421 - 490 VSGLGVIGRDRYGVFPLRGKILNVREASHKQIMENAEINNIIKIVGLQYKKSYDDAESLKTLRYGKIMIM 491 - 560 TDQDQDGSHIKGLLINFIHHNWPSLLKHGFLEEFITPIVKASKNKQELSFYSIPEFDEWKKHIENQKAWK 561 - 630 IKYYKGLGTSTAKEAKEYFADMERHRILFRYAGPEDDAAITLAFSKKKIDDRKEWLTNFMEDRRQRRLHG 631 - 700 LPEQFLYGTATKHLTYNDFINKELILFSNSDNERSIPSLVDGFKPGQRKVLFTCFKRNDKREVKVAQLAG 701 - 770 SVAEMSAYHHGEQALMMTIVNLAQNFVGSNNINLLQPIGQFGTRLHGGKDAASPRYIFTMLSTLARLLFP 771 - 840 AVDDNLLKFLYDDNQRVEPEWYIPIIPMVLINGAEGIGTGWACKLPNYDAREIVNNVRRMLDGLDPHPML 841 - 910 PNYKNFKGTIQELGQNQYAVSGEIFVVDRNTVEITELPVRTWTQVYKEQVLEPMLNGTDKTPALISDYKE 911 - 980 YHTDTTVKFVVKMTEEKLAQAEAAGLHKVFKLQTTLTCNSMVLFDHMGCLKKYETVQDILKEFFDLRLSY 981 - 1050 YGLRKEWLVGMLGAESTKLNNQARFILEKIQGKITIENRSKKDLIQMLVQRGYESDPVKAWKEAQEKAAE 1051 - 1120 EDETQNQHDDSSSDSGTPSGPDFNYILNMSLWSLTKEKVEELIKQRDAKGREVNDLKRKSPSDLWKEDLA 1121 - 1190 AFVEELDKVESQEREDVLAGMSGKAIKGKVGKPKVKKLQLEETMPSPYGRRIIPEITAMKADASKKLLKK 1191 - 1260 KKGDLDTAAVKVEFDEEFSGAPVEGAGEEALTPSVPINKGPKPKREKKEPGTRVRKTPTSSGKPSAKKVK 1261 - 1330 KRNPWSDDESKSESDLEETEPVVIPRDSLLRRAAAERPKYTFDFSEEEDDDADDDDDDNNDLEELKVKAS 1331 - 1400 PITNDGEDEFVPSDGLDKDEYTFSPGKSKATPEKSLHDKKSQDFGNLFSFPSYSQKSEDDSAKFDSNEED 1401 - 1470 SASVFSPSFGLKQTDKVPSKTVAAKKGKPSSDTVPKPKRAPKQKKVVEAVNSDSDSEFGIPKKTTTPKGK 1471 - 1540 GRGAKKRKASGSENEGDYNPGRKTSKTTSKKPKKTSFDQDSDVDIFPSDFPTEPPSLPRTGRARKEVKYF 1541 - 1610 AESDEEEDDVDFAMFN 1611 - 1626 //
