Ask about this productRelated genes to: HOXC11 antibody
- Gene:
- HOTAIR NIH gene
- Name:
- HOX transcript antisense RNA
- Previous symbol:
- -
- Synonyms:
- HOXC-AS4, HOXC11-AS1, NCRNA00072
- Chromosome:
- 12q13.13
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2008-06-04
- Date modifiied:
- 2016-12-01
- Gene:
- HOXC11 NIH gene
- Name:
- homeobox C11
- Previous symbol:
- HOX3H
- Synonyms:
- -
- Chromosome:
- 12q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-06
- Date modifiied:
- 2015-08-25
Related products to: HOXC11 antibody
Related articles to: HOXC11 antibody
- The cancer-promoting lncRNA HOTAIR has multiple isoforms. Which isoform of HOTAIR accounts for its expression and functions in cancer is unknown. Unlike HOTAIR's canonical intergenic isoform NR_003716 (HOTAIR-C), the novel isoform NR_047517 (HOTAIR-N) forms an overlapping antisense transcription locus with HOXC11. We identified HOTAIR-N as the dominant isoform that regulates the gene expression programs and networks for cell proliferation, survival, and death in cancer cells. The CpG island in the HOTAIR-N promoter was marked with epigenetic markers for active transcription. We identified a G-quadruplex (G4) motif rich region in the HOTAIR-N CpG island. Our findings indicate that G4s in HOTAIR-N CpG island is critical for expression of HOTAIR-N in cancer cells. Disruption of G4 may represent a novel therapeutic approach for cancer. The transcriptomes regulated by HOTAIR-N and Bloom in cancer cells as provided herein are important resources for the exploration of lncRNA, DNA helicases, and G4 in cancer. - Source: PubMed
Publication date: 2023/11/22
Qu XiaohanLin ZhenJayawickramarajah JanarthananAlsager John SSchmidt EmilyNephew Kenneth PFang FangBalasubramanian ShankarShan Bin - Arboleda-Tham Syndrome (ARTHS) is a rare genetic disorder caused by heterozygous, de novo mutations in Lysine(K) acetyltransferase 6A (KAT6A). ARTHS is clinically heterogeneous and characterized by several common features, including intellectual disability, developmental and speech delay, and hypotonia, and affects multiple organ systems. KAT6A is the enzymatic core of a histone-acetylation protein complex; however, the direct histone targets and gene regulatory effects remain unknown. In this study, we use ARTHS patient (n = 8) and control (n = 14) dermal fibroblasts and perform comprehensive profiling of the epigenome and transcriptome caused by KAT6A mutations. We identified differential chromatin accessibility within the promoter or gene body of 23% (14/60) of genes that were differentially expressed between ARTHS and controls. Within fibroblasts, we show a distinct set of genes from the posterior HOXC gene cluster (HOXC10, HOXC11, HOXC-AS3, HOXC-AS2, and HOTAIR) that are overexpressed in ARTHS and are transcription factors critical for early development body segment patterning. The genomic loci harboring HOXC genes are epigenetically regulated with increased chromatin accessibility, high levels of H3K23ac, and increased gene-body DNA methylation compared to controls, all of which are consistent with transcriptomic overexpression. Finally, we used unbiased proteomic mass spectrometry and identified two new histone post-translational modifications (PTMs) that are disrupted in ARTHS: H2A and H3K56 acetylation. Our multi-omics assays have identified novel histone and gene regulatory roles of KAT6A in a large group of ARTHS patients harboring diverse pathogenic mutations. This work provides insight into the role of KAT6A on the epigenomic regulation in somatic cell types. - Source: PubMed
Publication date: 2023/10/20
Singh MeghnaSpendlove Sarah JWei AngelaBondhus Leroy MNava Aileen Ade L Vitorino Francisca NAmano SethLee JacobEcheverria GeseniaGomez DianneGarcia Benjamin AArboleda Valerie A - Arboleda-Tham Syndrome (ARTHS) is a rare genetic disorder caused by heterozygous, truncating mutations in . ARTHS is clinically heterogeneous and characterized by several common features including intellectual disability, developmental and speech delay, hypotonia and affects multiple organ systems. is highly expressed in early development and plays a key role in cell-type specific differentiation. KAT6A is the enzymatic core of a histone-acetylation protein complex, however the direct histone targets and gene regulatory effects remain unknown. In this study, we use ARTHS patient (n=8) and control (n=14) dermal fibroblasts and perform comprehensive profiling of the epigenome and transcriptome caused by mutations. We identified differential chromatin accessibility within the promoter or gene body of 23%(14/60) of genes that were differentially expressed between ARTHS and controls. Within fibroblasts, we show a distinct set of genes from the posterior gene cluster (, HOXC-AS2, HOTAIR) that are overexpressed in ARTHS and are transcription factors critical for early development body segment patterning. The genomic loci harboring HOXC genes are epigenetically regulated with increased chromatin accessibility, high levels of H3K23ac, and increased gene-body DNA methylation compared to controls, all of which are consistent with transcriptomic overexpression. Finally, we used unbiased proteomic mass spectrometry and identified two new histone post-translational modifications (PTMs) that are disrupted in ARTHS: H2A and H3K56 acetylation. Our multi-omics assays have identified novel histone and gene regulatory roles of in a large group of ARTHS patients harboring diverse pathogenic mutations. This work provides insight into the role of KAT6A on the epigenomic regulation in somatic cell types. - Source: PubMed
Publication date: 2023/08/05
Singh MeghnaSpendlove SarahWei AngelaBondhus LeroyNava Aileende L Vitorino Francisca NAmano SethLee JacobEcheverria GeseniaGomez DianneGarcia Benjamin AArboleda Valerie A - Gastrointestinal cancers are the most common type of cancer affecting humans. High expression of HOX transcript antisense intergenic RNA (HOTAIR), a long noncoding RNA (lncRNA), in various types of different tumors may be associated with poor prognosis. In the present study, we performed a meta-analysis of the relationship between HOTAIR expression and gastrointestinal cancers. Five databases were comprehensively searched for all literature until January 2023. Moreover, the target genes of HOTAIR were predicted by coexpression analysis based on The Cancer Genome Atlas (TCGA) gene expression matrix for six gastrointestinal cancer types. Finally, the mechanism through which HOTAIR affects tumors of the digestive system was systematically reviewed. Our results showed that the high HOTAIR expression group had worse outcomes with a pooled hazard ratio (HR) of 1.56 (95% confidence interval [CI] = 1.38-1.75, P<0.001). Furthermore, HOTAIR was identified as an unfavorable prognostic factor for overall survival (OS) in the esophageal carcinoma (ESCA) and gastric cancer (GC), as the HR were 1.94 and 1.58, respectively. The high correlation between the expression of homeobox C (HOXC) family genes and HOTAIR, with correlation coefficients of 0.863 (HOXC11), 0.664 (HOXC10), 0.645 (HOXC8), and 0.581 (HOXC12). The 'cell cycle' pathway and pathways relating to infections, namely 'herpes simplex virus 1 infection' and 'complement and coagulation cascades' were significantly enriched in Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Also, we perform a systematic review to summarize the related oncogenic mechanism of HOTAIR. In conclusion, the HOTAIR has been identified as a potential prognostic factor in patients with gastrointestinal cancers. - Source: PubMed
Yang JinyouXu ShuyuWang ShaozhuoZou XuyanDuan MingxiuZhang QiaolingWang Chao - Gout is a disease caused by uric acid (UA) accumulation in the joints, causing inflammation. Two UA forms - monosodium urate (MSU) and soluble uric acid (sUA) have been shown to interact physically with inflammasomes, especially with the nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3), albeit the role of the immune response to UA is poorly understood, given that asymptomatic hyperuricemia does also exist. Macrophage phagocytosis of UA activate NLRP3, lead to cytokines release, and ultimately, lead to chemoattract neutrophils and lymphocytes to the gout flare joint spot. Genetic variants of inflammasome genes and of genes encoding their molecular partners may influence hyperuricemia and gout susceptibility, while also influencing other comorbidities such as metabolic syndrome and cardiovascular diseases. In this review, we summarize the inflammatory responses in acute and chronic gout, specifically focusing on innate immune cell mechanisms and genetic and epigenetic characteristics of participating molecules. Unprecedently, a novel UA binding protein - the neuronal apoptosis inhibitor protein (NAIP) - is suggested as responsible for the asymptomatic hyperuricemia paradox. β2-integrins: leukocyte-specific adhesion molecules; ABCG2: ATP-binding cassete family/breast cancer-resistant protein; ACR: American college of rheumatology; AIM2: absent in melanoma 2, type of pattern recognition receptor; ALPK1: alpha-protein kinase 1; ANGPTL2: angiopoietin-like protein 2; ASC: apoptosis-associated speck-like protein; BIR: baculovirus inhibitor of apoptosis protein repeat; BIRC1: baculovirus IAP repeat-containing protein 1; BIRC2: baculoviral IAP repeat-containing protein 2; C5a: complement anaphylatoxin; cAMP: cyclic adenosine monophosphate; CARD: caspase activation and recruitment domains; CARD8: caspase recruitment domain-containing protein 8; CASP1: caspase 1; CCL3: chemokine (C-C motif) ligand 3; CD14: cluster of differentiation 14; CD44: cluster of differentiation 44; Cg05102552: DNA-methylation site, usually cytosine followed by guanine nucleotides; contains arbitrary identification code; CIDEC: cell death-inducing DNA fragmentation factor-like effector family; CKD: chronic kidney disease; CNV: copy number variation; CPT1A: carnitine palmitoyl transferase - type 1a; CXCL1: chemokine (CXC motif) ligand 1; DAMPs: damage associated molecular patterns; DC: dendritic cells; DNMT(1): maintenance DNA methyltransferase; eQTL: expression quantitative trait loci; ERK1: extracellular signal-regulated kinase 1; ERK2: extracellular signal-regulated kinase 2; EULAR: European league against rheumatism; GMCSF: granulocyte-macrophage colony-stimulating factor; GWAS: global wide association studies; H3K27me3: tri-methylation at the 27th lysine residue of the histone h3 protein; H3K4me1: mono-methylation at the 4th lysine residue of the histone h3 protein; H3K4me3: tri-methylation at the 4th lysine residue of the histone h3 protein; HOTAIR: human gene located between hoxc11 and hoxc12 on chromosome 12; IκBα: cytoplasmatic protein/Nf-κb transcription inhibitor; IAP: inhibitory apoptosis protein; IFNγ: interferon gamma; IL-1β: interleukin 1 beta; IL-12: interleukin 12; IL-17: interleukin 17; IL18: interleukin 18; IL1R1: interleukin-1 receptor; IL-1Ra: interleukin-1 receptor antagonist; IL-22: interleukin 22; IL-23: interleukin 23; IL23R: interleukin 23 receptor; IL-33: interleukin 33; IL-6: interleukin 6; IMP: inosine monophosphate; INSIG1: insulin-induced gene 1; JNK1: c-jun n-terminal kinase 1; lncRNA: long non-coding ribonucleic acid; LRR: leucine-rich repeats; miR: mature non-coding microRNAs measuring from 20 to 24 nucleotides, animal origin; miR-1: miR followed by arbitrary identification code; miR-145: miR followed by arbitrary identification code; miR-146a: miR followed by arbitrary identification code, "a" stands for mir family; "a" family presents similar mir sequence to "b" family, but different precursors; miR-20b: miR followed by arbitrary identification code; "b" stands for mir family; "b" family presents similar mir sequence to "a" family, but different precursors; miR-221: miR - followed by arbitrary identification code; miR-221-5p: miR followed by arbitrary identification code; "5p" indicates different mature miRNAs generated from the 5' arm of the pre-miRNA hairpin; miR-223: miR followed by arbitrary identification code; miR-223-3p: mir followed by arbitrary identification code; "3p" indicates different mature miRNAs generated from the 3' arm of the pre-miRNA hairpin; miR-22-3p: miR followed by arbitrary identification code, "3p" indicates different mature miRNAs generated from the 3' arm of the pre-miRNA hairpin; MLKL: mixed lineage kinase domain-like pseudo kinase; MM2P: inductor of m2-macrophage polarization; MSU: monosodium urate; mTOR: mammalian target of rapamycin; MyD88: myeloid differentiation primary response 88; n-3-PUFAs: n-3-polyunsaturated fatty-acids; NACHT: acronym for NAIP (neuronal apoptosis inhibitor protein), C2TA (MHC class 2 transcription activator), HET-E (incompatibility locus protein from podospora anserina) and TP1 (telomerase-associated protein); NAIP: neuronal apoptosis inhibitory protein (human); Naip1: neuronal apoptosis inhibitory protein type 1 (murine); Naip5: neuronal apoptosis inhibitory protein type 5 (murine); Naip6: neuronal apoptosis inhibitory protein type 6 (murine); NBD: nucleotide-binding domain; Nek7: smallest NIMA-related kinase; NET: neutrophil extracellular traps; Nf-κB: nuclear factor kappa-light-chain-enhancer of activated b cells; NFIL3: nuclear-factor, interleukin 3 regulated protein; NIIMA: network of immunity in infection, malignancy, and autoimmunity; NLR: nod-like receptor; NLRA: nod-like receptor NLRA containing acidic domain; NLRB: nod-like receptor NLRA containing BIR domain; NLRC: nod-like receptor NLRA containing CARD domain; NLRC4: nod-like receptor family CARD domain containing 4; NLRP: nod-like receptor NLRA containing PYD domain; NLRP1: nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain containing 1; NLRP12: nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain containing 12; NLRP3: nod-like receptor family pyrin domain containing 3; NOD2: nucleotide-binding oligomerization domain; NRBP1: nuclear receptor-binding protein; Nrf2: nuclear factor erythroid 2-related factor 2; OR: odds ratio; P2X: group of membrane ion channels activated by the binding of extracellular; P2X7: p2x purinoceptor 7 gene; p38: member of the mitogen-activated protein kinase family; PAMPs: pathogen associated molecular patters; PBMC: peripheral blood mononuclear cells; PGGT1B: geranylgeranyl transferase type-1 subunit beta; PHGDH: phosphoglycerate dehydrogenase; PI3-K: phospho-inositol; PPARγ: peroxisome proliferator-activated receptor gamma; PPARGC1B: peroxisome proliferative activated receptor, gamma, coactivator 1 beta; PR3: proteinase 3 antigen; Pro-CASP1: inactive precursor of caspase 1; Pro-IL1β: inactive precursor of interleukin 1 beta; PRR: pattern recognition receptors; PYD: pyrin domain; RAPTOR: regulatory associated protein of mTOR complex 1; RAS: renin-angiotensin system; REDD1: regulated in DNA damage and development 1; ROS: reactive oxygen species; rs000*G: single nuclear polymorphism, "*G" is related to snp where replaced nucleotide is guanine, usually preceded by an id number; SLC2A9: solute carrier family 2, member 9; SLC7A11: solute carrier family 7, member 11; SMA: smooth muscular atrophy; Smac: second mitochondrial-derived activator of caspases; SNP: single nuclear polymorphism; Sp3: specificity protein 3; ST2: serum stimulation-2; STK11: serine/threonine kinase 11; sUA: soluble uric acid; Syk: spleen tyrosine kinase; TAK1: transforming growth factor beta activated kinase; Th1: type 1 helper T cells; Th17: type 17 helper T cells; Th2: type 2 helper T cells; Th22: type 22 helper T cells; TLR: tool-like receptor; TLR2: toll-like receptor 2; TLR4: toll-like receptor 4; TNFα: tumor necrosis factor alpha; TNFR1: tumor necrosis factor receptor 1; TNFR2: tumor necrosis factor receptor 2; UA: uric acid; UBAP1: ubiquitin associated protein; ULT: urate-lowering therapy; URAT1: urate transporter 1; VDAC1: voltage-dependent anion-selective channel 1. - Source: PubMed
Publication date: 2023/02/06
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