Human Gene ING3 (ENST00000315870.10) from GENCODE V44
Description: Homo sapiens inhibitor of growth family member 3 (ING3), transcript variant 1, mRNA. (from RefSeq NM_019071) RefSeq Summary (NM_019071): The protein encoded by this gene is similar to ING1, a tumor suppressor protein that can interact with TP53, inhibit cell growth, and induce apoptosis. This protein contains a PHD-finger, which is a common motif in proteins involved in chromatin remodeling. This gene can activate p53 trans-activated promoters, including promoters of p21/waf1 and bax. Overexpression of this gene has been shown to inhibit cell growth and induce apoptosis. Allelic loss and reduced expression of this gene were detected in head and neck cancers. Two alternatively spliced transcript variants encoding different isoforms have been observed. [provided by RefSeq, Jul 2008]. Gencode Transcript: ENST00000315870.10 Gencode Gene: ENSG00000071243.16 Transcript (Including UTRs) Position: hg38 chr7:120,950,777-120,977,216 Size: 26,440 Total Exon Count: 12 Strand: + Coding Region Position: hg38 chr7:120,950,897-120,974,844 Size: 23,948 Coding Exon Count: 12
ID:ING3_HUMAN DESCRIPTION: RecName: Full=Inhibitor of growth protein 3; AltName: Full=p47ING3; FUNCTION: Component of the NuA4 histone acetyltransferase (HAT) complex which is involved in transcriptional activation of select genes principally by acetylation of nucleosomal histones H4 and H2A. This modification may both alter nucleosome - DNA interactions and promote interaction of the modified histones with other proteins which positively regulate transcription. This complex may be required for the activation of transcriptional programs associated with oncogene and proto-oncogene mediated growth induction, tumor suppressor mediated growth arrest and replicative senescence, apoptosis, and DNA repair. NuA4 may also play a direct role in DNA repair when directly recruited to sites of DNA damage. SUBUNIT: Interacts with H3K4me3 and to a lesser extent with H3K4me2. Component of the NuA4 histone acetyltransferase complex which contains the catalytic subunit KAT5/TIP60 and the subunits EP400, TRRAP/PAF400, BRD8/SMAP, EPC1, DMAP1/DNMAP1, RUVBL1/TIP49, RUVBL2, ING3, actin, ACTL6A/BAF53A, MORF4L1/MRG15, MORF4L2/MRGX, MRGBP, YEATS4/GAS41, VPS72/YL1 and MEAF6. The NuA4 complex interacts with MYC and the adenovirus E1A protein. HTATTIP/TIP60, EPC1, and ING3 together constitute a minimal HAT complex termed Piccolo NuA4. SUBCELLULAR LOCATION: Nucleus. TISSUE SPECIFICITY: Expressed in brain, heart, kidney, liver, lung, ovaries, placenta, prostate, skeletal muscle, small intestine, spleen, testis and thymus. DOMAIN: The PHD-type zinc finger mediates the binding to H3K4me3. DISEASE: Defects in ING3 may be a cause of head and neck squamous cell carcinomas (HNSCC) [MIM:275355]; also known as squamous cell carcinoma of the head and neck. SIMILARITY: Belongs to the ING family. SIMILARITY: Contains 1 PHD-type zinc finger. SEQUENCE CAUTION: Sequence=AAF28979.1; Type=Frameshift; Positions=90; Sequence=AAH73865.1; Type=Miscellaneous discrepancy; Note=Intron retention;
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on Q9NXR8
Front
Top
Side
The pictures above may be empty if there is no ModBase structure for the protein. The ModBase structure frequently covers just a fragment of the protein. You may be asked to log onto ModBase the first time you click on the pictures. It is simplest after logging in to just click on the picture again to get to the specific info on that model.
Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.
US Server
