8h0i: Difference between revisions

Line 8:

<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=8h0i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8h0i OCA], [https://pdbe.org/8h0i PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8h0i RCSB], [https://www.ebi.ac.uk/pdbsum/8h0i PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8h0i ProSAT]</span></td></tr>

</table>

~~== Disease ==~~

[https://www.uniprot.org/uniprot/PEBB_HUMAN PEBB_HUMAN] Note=A chromosomal aberration involving CBFB is associated with acute myeloid leukemia of M4EO subtype. Pericentric inversion inv(16)(p13;q22). The inversion produces a fusion protein that consists of the 165 N-terminal residues of CBF-beta (PEPB2) with the tail region of MYH11.

== Function ==

[https://www.uniprot.org/uniprot/~~PEBB_HUMAN PEBB_HUMAN~~] ~~CBF binds~~ to the ~~core site~~, 5'-~~PYGPYGGT~~-3', of a ~~number~~ of ~~enhancers and promoters~~, ~~including murine leukemia virus~~, ~~polyomavirus enhancer, T-cell receptor enhancers, LCK, IL3~~ and ~~GM-CSF promoters. CBFB enhances DNA binding by RUNX1~~.

[https://www.uniprot.org/uniprot/ABC3G_HUMAN ABC3G_HUMAN] DNA deaminase (cytidine deaminase) that mediates a form of innate resistance to retroviral infections (at least to HIV-1 infection) by triggering G-to-A hypermutation in the newly synthesized viral DNA. The replacements C-to-U in the minus strand DNA of HIV-1 during reverse transcription, leads to G-to-A transitions in the plus strand. The inhibition of viral replication is either due to the degradation of the minus strand before its integration or to the lethality of the hypermutations. Modification of both DNA strands is not excluded. This antiviral activity is neutralized by the virion infectivity factor (VIF), that prevents the incorporation of APOBEC3G into progeny HIV-1 virions by both inhibiting its translation and/or by inducing its ubiquitination and subsequent degradation by the 26S proteasome. May also prevent the transposition of a subset of retroelements. Binds a variety of RNAs, but does not display detectable APOB, NF1 and NAT1 mRNA editing.<ref>PMID:14557625</ref> <ref>PMID:12167863</ref> <ref>PMID:12808466</ref> <ref>PMID:12809610</ref> <ref>PMID:12808465</ref> <ref>PMID:12859895</ref> <ref>PMID:12970355</ref> <ref>PMID:14528300</ref> <ref>PMID:15031497</ref> <ref>PMID:16527742</ref> <ref>PMID:21123384</ref> <ref>PMID:18288108</ref>

== Publication Abstract from PubMed ==

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@@ Line 8: / Line 8: @@
 <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=8h0i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8h0i OCA], [https://pdbe.org/8h0i PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8h0i RCSB], [https://www.ebi.ac.uk/pdbsum/8h0i PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8h0i ProSAT]</span></td></tr>
 </table>
-== Disease ==
-[https://www.uniprot.org/uniprot/PEBB_HUMAN PEBB_HUMAN] Note=A chromosomal aberration involving CBFB is associated with acute myeloid leukemia of M4EO subtype. Pericentric inversion inv(16)(p13;q22). The inversion produces a fusion protein that consists of the 165 N-terminal residues of CBF-beta (PEPB2) with the tail region of MYH11.
 == Function ==
-[https://www.uniprot.org/uniprot/PEBB_HUMAN PEBB_HUMAN] CBF binds to the core site, 5'-PYGPYGGT-3', of a number of enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T-cell receptor enhancers, LCK, IL3 and GM-CSF promoters. CBFB enhances DNA binding by RUNX1.
+[https://www.uniprot.org/uniprot/ABC3G_HUMAN ABC3G_HUMAN] DNA deaminase (cytidine deaminase) that mediates a form of innate resistance to retroviral infections (at least to HIV-1 infection) by triggering G-to-A hypermutation in the newly synthesized viral DNA. The replacements C-to-U in the minus strand DNA of HIV-1 during reverse transcription, leads to G-to-A transitions in the plus strand. The inhibition of viral replication is either due to the degradation of the minus strand before its integration or to the lethality of the hypermutations. Modification of both DNA strands is not excluded. This antiviral activity is neutralized by the virion infectivity factor (VIF), that prevents the incorporation of APOBEC3G into progeny HIV-1 virions by both inhibiting its translation and/or by inducing its ubiquitination and subsequent degradation by the 26S proteasome. May also prevent the transposition of a subset of retroelements. Binds a variety of RNAs, but does not display detectable APOB, NF1 and NAT1 mRNA editing.<ref>PMID:14557625</ref> <ref>PMID:12167863</ref> <ref>PMID:12808466</ref> <ref>PMID:12809610</ref> <ref>PMID:12808465</ref> <ref>PMID:12859895</ref> <ref>PMID:12970355</ref> <ref>PMID:14528300</ref> <ref>PMID:15031497</ref> <ref>PMID:16527742</ref> <ref>PMID:21123384</ref> <ref>PMID:18288108</ref>
 <div style="background-color:#fffaf0;">
 == Publication Abstract from PubMed ==