| Name | H3 clustered histone 10 |
| Description | Histones are basic nuclear proteins that are responsible for the nucleosome structure of the chromosomal fiber in eukaryotes. Two molecules of each of the four core histones (H2A, H2B, H3, and H4) form an octamer, around which approximately 146 bp of DNA is wrapped in repeating units, called nucleosomes. The linker histone, H1, interacts with linker DNA between nucleosomes and functions in the compaction of chromatin into higher order structures. This gene is intronless and encodes a replication-dependent histone that is a member of the histone H3 family. Transcripts from this gene lack polyA tails but instead contain a palindromic termination element. This gene is found in the small histone gene cluster on chromosome 6p22-p21.3. [provided by RefSeq, Aug 2015] |
| Summary |
{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Histone H3 variants—including those encoded by the HIST1 gene cluster such as HIST1H3C—play critical roles in regulating chromatin structure and function. Studies in pediatric high‐grade gliomas, particularly diffuse intrinsic pontine glioma (DIPG) and glioblastoma, have demonstrated that specific point mutations (for example, a lysine‐to‐methionine substitution at position 27) in histone H3.3 and its close replication‐independent counterpart, histone H3.1 (to which HIST1H3C is related), define distinct oncogenic subgroups with profound prognostic and therapeutic implications."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " These mutations are not only associated with a striking global reduction in H3K27 trimethylation—a key repressive chromatin mark—but also with local retention of H3K27me3 at tumor suppressor loci, leading to their silencing and contributing to tumor progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In addition to mutational events, the proper deposition of H3 variants is governed by histone chaperones such as DAXX, ATRX, and other chromatin assembly factors that enable replication‐independent incorporation into chromatin. This regulated deposition is important for maintaining gene expression programs by marking active chromatin regions and safeguarding genome integrity."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " Moreover, distinct histone H3 variants are linked to cell type–specific transcriptional programs and may even exhibit tumor type specificity; for example, driver alterations in H3.3 and H3.1 differentially affect chondroblastomas, giant cell tumors of bone, and midline gliomas."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n A related epigenetic mechanism is highlighted by studies in neuroblastoma, where methylation changes in promoter regions of HIST1H3C have been associated with classical risk factors and correlate with overall survival, suggesting that beyond mutational events, epigenetic regulation of H3-encoding genes is central to disease stratification."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " Together, these findings emphasize that histone H3 variants—including those encoded by HIST1H3C—are multifunctional regulators of chromatin dynamics, gene expression, DNA repair, and cell cycle progression. Their mutation or epigenetic alteration not only reprograms the epigenome but also drives oncogenic processes in a tumor type–specific manner.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Dong-Anh Khuong-Quang, Pawel Buczkowicz, Patricia Rakopoulos, et al. "}, {"type": "b", "children": [{"type": "t", "text": "K27M mutation in histone H3.3 defines clinically and biologically distinct subgroups of pediatric diffuse intrinsic pontine gliomas."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Acta Neuropathol (2012)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s00401-012-0998-0"}], "href": "https://doi.org/10.1007/s00401-012-0998-0"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "22661320"}], "href": "https://pubmed.ncbi.nlm.nih.gov/22661320"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "David Castel, Cathy Philippe, Raphaël Calmon, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Histone H3F3A and HIST1H3B K27M mutations define two subgroups of diffuse intrinsic pontine gliomas with different prognosis and phenotypes."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Acta Neuropathol (2015)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s00401-015-1478-0"}], "href": "https://doi.org/10.1007/s00401-015-1478-0"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26399631"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26399631"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Sriram Venneti, Mihir T Garimella, Lisa M Sullivan, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Evaluation of histone 3 lysine 27 trimethylation (H3K27me3) and enhancer of Zest 2 (EZH2) in pediatric glial and glioneuronal tumors shows decreased H3K27me3 in H3F3A K27M mutant glioblastomas."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Brain Pathol (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1111/bpa.12042"}], "href": "https://doi.org/10.1111/bpa.12042"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "23414300"}], "href": "https://pubmed.ncbi.nlm.nih.gov/23414300"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Sriram Venneti, Mariarita Santi, Michelle Madden Felicella, et al. "}, {"type": "b", "children": [{"type": "t", "text": "A sensitive and specific histopathologic prognostic marker for H3F3A K27M mutant pediatric glioblastomas."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Acta Neuropathol (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s00401-014-1338-3"}], "href": "https://doi.org/10.1007/s00401-014-1338-3"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "25200322"}], "href": "https://pubmed.ncbi.nlm.nih.gov/25200322"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Pascal Drané, Khalid Ouararhni, Arnaud Depaux, et al. "}, {"type": "b", "children": [{"type": "t", "text": "The death-associated protein DAXX is a novel histone chaperone involved in the replication-independent deposition of H3.3."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Genes Dev (2010)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1101/gad.566910"}], "href": "https://doi.org/10.1101/gad.566910"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "20504901"}], "href": "https://pubmed.ncbi.nlm.nih.gov/20504901"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Sam Behjati, Patrick S Tarpey, Nadège Presneau, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Distinct H3F3A and H3F3B driver mutations define chondroblastoma and giant cell tumor of bone."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Nat Genet (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/ng.2814"}], "href": "https://doi.org/10.1038/ng.2814"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24162739"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24162739"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Pawel Buczkowicz, Christine Hoeman, Patricia Rakopoulos, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Genomic analysis of diffuse intrinsic pontine gliomas identifies three molecular subgroups and recurrent activating ACVR1 mutations."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Nat Genet (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/ng.2936"}], "href": "https://doi.org/10.1038/ng.2936"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24705254"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24705254"}]}, {"type": "r", "ref": 8, "children": [{"type": "t", "text": "Anneleen Decock, Maté Ongenaert, Jasmien Hoebeeck, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Genome-wide promoter methylation analysis in neuroblastoma identifies prognostic methylation biomarkers."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Genome Biol (2012)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1186/gb-2012-13-10-r95"}], "href": "https://doi.org/10.1186/gb-2012-13-10-r95"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "23034519"}], "href": "https://pubmed.ncbi.nlm.nih.gov/23034519"}]}]}]}
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| NCBI Gene ID | 8357 |
| API | |
| Download Associations | |
| Predicted Functions |
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| Co-expressed Genes |
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| Expression in Tissues and Cell Lines |
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H3C10 has 689 functional associations with biological entities spanning 4 categories (disease, phenotype or trait, functional term, phrase or reference, cell line, cell type or tissue, gene, protein or microRNA) extracted from 10 datasets.
Click the + buttons to view associations for H3C10 from the datasets below.
If available, associations are ranked by standardized value
| Dataset | Summary | |
|---|---|---|
| Allen Brain Atlas Aging Dementia and Traumatic Brain Injury Tissue Sample Gene Expression Profiles | tissue samples with high or low expression of H3C10 gene relative to other tissue samples from the Allen Brain Atlas Aging Dementia and Traumatic Brain Injury Tissue Sample Gene Expression Profiles dataset. | |
| CM4AI KOLF21J CRISPRi Gene Perturbation Atlas | gene perturbations changing expression of H3C10 gene from the CM4AI KOLF21J CRISPRi Gene Perturbation Atlas dataset. | |
| DISEASES Experimental Gene-Disease Association Evidence Scores 2025 | diseases associated with H3C10 gene in GWAS datasets from the DISEASES Experimental Gene-Disease Assocation Evidence Scores 2025 dataset. | |
| DISEASES Text-mining Gene-Disease Association Evidence Scores 2025 | diseases co-occuring with H3C10 gene in abstracts of biomedical publications from the DISEASES Text-mining Gene-Disease Assocation Evidence Scores 2025 dataset. | |
| GTEx Tissue Gene Expression Profiles 2023 | tissues with high or low expression of H3C10 gene relative to other tissues from the GTEx Tissue Gene Expression Profiles 2023 dataset. | |
| GTEx Tissue-Specific Aging Signatures | tissue samples with high or low expression of H3C10 gene relative to other tissue samples from the GTEx Tissue-Specific Aging Signatures dataset. | |
| Replogle et al., Cell, 2022 K562 Essential Perturb-seq Gene Perturbation Signatures | gene perturbations changing expression of H3C10 gene from the Replogle et al., Cell, 2022 K562 Essential Perturb-seq Gene Perturbation Signatures dataset. | |
| Replogle et al., Cell, 2022 K562 Genome-wide Perturb-seq Gene Perturbation Signatures | gene perturbations changing expression of H3C10 gene from the Replogle et al., Cell, 2022 K562 Genome-wide Perturb-seq Gene Perturbation Signatures dataset. | |
| Rummagene Transcription Factor Associations 2026 | transcription factors regulating expression of H3C10 gene from the Rummagene Transcription Factor Associations 2026 dataset. | |
| WikiPathways Pathways 2024 | pathways involving H3C10 protein from the WikiPathways Pathways 2024 dataset. | |