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CHD5 (chromodomain helicase DNA binding protein 5)

Written2012-01Venkatadri Kolla, Mayumi Higashi, Tiangang Zhuang, Garrett M Brodeur
Children's Hospital of Philadelphia, Oncology Research, CTRB Rm 3018, 3501 Civic Center Blvd, Philadelphia, PA 19104, USA
This article is an update of :
2010-01Garrett M Brodeur, Peter S White
Children's Hospital of Philadelphia, Oncology Research, CTRB Rm 3018, 3501 Civic Center Blvd, Philadelphia, PA 19104, USA (GMB); Children's Hospital of Philadelphia, Center for Biomedical Informatics, Rm 1407 CHOP North, 34th St, Civic Center Blvd, Philadelphia, PA 19104, USA (PSW)

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Alias (NCBI)DKFZp434N231
HGNC (Hugo) CHD5
LocusID (NCBI) 26038
Atlas_Id 44521
Location 1p36.31  [Link to chromosome band 1p36]
Location_base_pair Starts at 6101787 and ends at 6180321 bp from pter ( according to GRCh38/hg38-Dec_2013)  [Mapping CHD5.png]
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)
AGBL5 (2p23.3)::CHD5 (1p36.31)


Description Gene is encoded by 42 exons, spanning 78331 bp (NCBI).
mRNA: NM_015557.2.
Transcription The CHD5 cDNA sequence spans 9646 bp, with a 5' UTR of 100 bp, a single open reading frame of 5865 bp, and a 3' UTR of 3681 bp (Thompson et al., 2003).
Pseudogene None known.


  The functional domains of the chromodomain-helicase-DNA binding protein 5 (CHD5) are shown above. There are two PHD type zinc fingers, two chromodomains, a split DEAH-box ATP-helicase domain, and a poorly defined DNA binding domain (NP_056372.1).
Description The 5' portion of CHD5 is predicted to contain two zinc-fingers of the PHD class (amino-acid positions 345-390 and 418-463), followed closely by two chromodomains (510-525 and 596-625). PHD zinc-finger motifs are thought to play roles in chromatin-associated transcriptional regulation, whereas chromodomains are frequently observed in proteins involved in recruitment of transcriptional regulatory complexes. The central portion of the protein includes a predicted DEAH-box type helicase domain (703-999) and a putative SNF2 domain (1054-1138). DEAH ATP helicases are ATP-dependent and are usually associated with nucleic acid unwinding. SNF2 domains are commonly observed in, although not restricted to, proteins involved in chromatin unwinding, DNA repair and recombination, and transcriptional regulation. A number of potential nuclear localization signals are also present (50-67, 54-71, 97-114, 100-117, 240-257, 253-270, 918-935) (Thompson et al., 2003).
Expression Detectable expression of CHD5 was limited to all neural-derived tissues (fetal brain, total brain, cerebellum) and adrenal gland, with no expression detected in placenta, liver, fetal liver, spleen, bone marrow, thyroid, thymus, salivary gland, stomach, pancreas, small intestine, colon, or prostate (Thompson et al., 2003; Okawa et al., 2008; Wikimedia Commons). Expression is also found in testis (Potts et al., 2011; BioGPS; Brodeur, unpublished observations).
Localisation Intracellular expression is preferentially nuclear (Brodeur, unpublished observations).
Function CHD family proteins are thought to play a role in chromatin remodeling. CHD5 is most homologous to CHD3 and CHD4, which participate in the formation of a nucleosome remodeling and deacetylation (NuRD) complex, in association with other proteins. This complex is generally thought to repress transcription.
Homology Strongest homology is to CHD3 and CHD4, with weaker homology to CHD1, CHD2, CHD6, CHD7, CHD8 and CHD9.


Note No examples of homozygous inactivation have been identified, and no nonsense or frameshift mutations have been identified in any cancers to date. Several missense mutations have been detected, but it is unclear if any of these have an effect on the function of the protein (Okawa et al., 2008; Fujita et al., 2008; Ng et al., 2008; Koyama et al., 2012).

Implicated in

Entity Neuroblastoma
Note CHD5, a new member of the chromodomain gene family, is preferentially expressed in the nervous system (Thompson et al., 2003). CHD5 maps to 1p36.3, a region of consistent deletion in neuroblastoma and other tumors (White et al., 2005). CHD5 is one of 23 genes that map to the 800 kb region of consistent deletion on 1p36.3 in an analysis of over 1200 primary neuroblastomas (Okawa et al., 2008). Functional analysis of CHD5 after transfection into neuroblastoma cell lines demonstrates that CHD5 functions as a tumor suppressor gene, suppressing both clonogenicity and tumorigenicity. The promoter was methylated especially between -780 and -450 in neuroblastoma cell lines with 1p36 deletions, but not those with two copies of CHD5. Furthermore, high CHD5 expression is highly correlated with favorable clinical and biological risk features as well as outcome in a panel of 101 primary tumors (Fujita et al., 2008). These data suggest that CHD5 is a bona fide tumor suppressor gene in neuroblastomas. Deletion of 1p36 is associated with loss of CHD5 expression, and the CHD5 promoter is preferentially methylated in lines with 1p36 deletion. Low CHD5 expression is also associated with a worse outcome in neuroblastoma patients. Furthermore, low CHD5 expression is associated with a worse outcome in neuroblastoma patients (Koyama et al., 2012). Most recent protein expression studies showed that CHD5 acted as immunohistochemical marker in NB in 90 primary NTs suggesting a strong association of CHD5 expression with favorable prognostic variables that were tested in a blind set of 32 NB tumors (Garcia et al., 2010). In addition to these observations this brain specific protein has been shown to regulate neural gene expression (Potts et al., 2011). Moreover, CHD5 forms a NuRD complex similar to Mi2β/CHD4, and it presumably acts as chromatin remodeling enzyme in regulating gene expression (Kolla et al., unpublished observations).
Entity Gliomas
Note CHD5 is one of several genes that maps to the 700 kb region of consistent deletion in 17 glioma cell lines (Law et al., 2005). Loss of CHD5 expression is associated with deletion of 1p36 in a panel of 54 glial tumors (Bagchi et al., 2007). These data are consistent with a role for CHD5 as a tumor suppressor gene in these tumors.
Entity Melanoma
Note A subset of malignant melanoma families show linkage to 1p36, and CHD5 is a tumor suppressor gene that maps to this region. However, screening of CHD5 for mutations in eight melanoma-prone families linked to 1p36 revealed no deleterious coding or splice site mutations (Ng et al., 2008). Moreover, to understand the role of CHD5 in familial melanoma, studies have shown CHD5 variants in familial cutaneous melanoma that could block or alter the ability of CHD5 to regulate the cell cycle pathway and to effect cellular control. But only one out of 47 families studied has this variant. Thus, it appears to be a rare event and further elaborative studies are required to confirm the role of CHD5 in melanoma pathogenesis (Lang et al., 2011). This suggests that CHD5 is not a major melanoma or subcutaneous melanoma susceptibility gene, at least in the families screened.
Entity Ovarian cancer
Note Mutation and methylation analysis of CHD5 gene was undertaken in 123 ovarian cancers, whereas no such mutations were identified in 60 primary breast cancers. Somatic heterozygous missense mutations were identified in 3 samples, and promoter methylation was identified in another 3 of 45 samples tested (Gorringe et al., 2008). Recently, correlation of CHD5 with clinicopathological features of the tumor is also shown by quantitative RT-PCR methods. CHD5 is downregulated in a certain number of ovarian cancers and appears to be an adverse predictor candidate of ovarian cancer disease-free and total survival (Wong et al., 2011). These data suggest that CHD5 may play a role as a tumor suppressor gene in a subset of ovarian cancers, but there may be other suppressors on 1p36 as well.
Entity Colorectal cancer
Note The methylation status of a set of cancer-related genes was studied in 102 colon cancers from Iranian and African-American populations (51 each). The methylation status of the promoters of three genes (CHD5, ICAM5 and GPNMB) was significantly higher in cancers from the African-American population compared to the Iranian patients (Mokarram et al., 2009). This suggests that these genes may play a role in the incidence or aggressiveness of colorectal cancer in this population.
Entity Gastric cancer
Note The methylation status of the CHD5 promoter was examined in 15 primary gastric cancers and 7 gastric cancer cell lines. CHD5 expression was downregulated in 7/7 cell lines, and methylation of the promoter was found in all 7 lines, and a similar correlation was found in 11/15 primary tumors. Ectopic expression of CHD5 led to significant growth inhibition. These results suggest that CHD5 plays a role as a tumor suppressor gene in gastric cancer, and its expression may be down-regulated epigenetically.
Entity Various cancers (colon cancer, breast cancer, gliomas)
Note The promoter of all nine current members of the CHD family were analyzed for methylation, and only the CHD5 promoter showed CpG hypermethylation in a subset of primary cancers, especially colon cancer, breast cancer and gliomas (Mulero-Navarro and Esteller, 2008). Thus, epigenetic inactivation of CHD5 expression may contribute to the pathogenesis of various cancers.
Entity Lung cancer
Note Role of CHD5 in a lung cancer and epigenetic modification as well as its tumor-suppressive capability has been studied by measuring CHD5 mRNA and protein expression in lung cancer cells and tissues. CHD5 expression ranged from low to absent in the lung cancer cell lines and tissues examined correlated the results with CHD5 promoter hypermethylation. Clonogenicity and tumor growth were abrogated in lung cancer cell lines A549 and H1299 upon restoration of CHD5 expression (Zhao et al., 2011). These results suggest that CHD5 serves as a potential tumor suppressor gene in lung cancer that is inactivated via an epigenetic mechanism.
Entity Prostate cancer
Note Comprehensive genomic survey has been conducted for somatic events in systemic metastatic prostate tumors using both high-resolution copy number analysis and targeted mutational survey of 3508 exons from 577 cancer-related genes using next generation sequencing. Novel somatic point mutations have been shown in CHD5 along with MTOR, BRCA2, and ARHGEF12 (Robbins et al., 2011). This study indicates a deep genomic analysis of advanced metastatic prostate tumors that lead to somatic alterations, possibly contributing to lethal prostate cancer.
Entity Laryngeal squamous cell carcinoma
Note Tumor suppressive role of CHD5 has been observed in 65 patients with laryngeal squamous cell carcinomas (LSCC) where both CHD5 RNA and protein expressions were significantly lower. These observations were also in correlation with promoter hypermethylation. Interestingly, ectopic expression of CHD5 in laryngeal cancer cells led to significant inhibition of growth and invasiveness (Wang et al., 2011). These data suggest that CHD5 acts as a tumor suppressor gene that is epigenetically downregulated in LSCC.


Note None known.


CHD5 is a tumor suppressor at human 1p36.
Bagchi A, Papazoglu C, Wu Y, Capurso D, Brodt M, Francis D, Bredel M, Vogel H, Mills AA.
Cell. 2007 Feb 9;128(3):459-75.
PMID 17289567
MicroRNA-211 expression promotes colorectal cancer cell growth in vitro and in vivo by targeting tumor suppressor CHD5.
Cai C, Ashktorab H, Pang X, Zhao Y, Sha W, Liu Y, Gu X.
PLoS One. 2012;7(1):e29750. Epub 2012 Jan 3.
PMID 22235338
CHD5, a tumor suppressor gene deleted from 1p36.31 in neuroblastomas.
Fujita T, Igarashi J, Okawa ER, Gotoh T, Manne J, Kolla V, Kim J, Zhao H, Pawel BR, London WB, Maris JM, White PS, Brodeur GM.
J Natl Cancer Inst. 2008 Jul 2;100(13):940-9. Epub 2008 Jun 24.
PMID 18577749
Expression of the neuron-specific protein CHD5 is an independent marker of outcome in neuroblastoma.
Garcia I, Mayol G, Rodriguez E, Sunol M, Gershon TR, Rios J, Cheung NK, Kieran MW, George RE, Perez-Atayde AR, Casala C, Galvan P, de Torres C, Mora J, Lavarino C.
Mol Cancer. 2010 Oct 15;9:277.
PMID 20950435
Mutation and methylation analysis of the chromodomain-helicase-DNA binding 5 gene in ovarian cancer.
Gorringe KL, Choong DY, Williams LH, Ramakrishna M, Sridhar A, Qiu W, Bearfoot JL, Campbell IG.
Neoplasia. 2008 Nov;10(11):1253-8.
PMID 18953434
Complex constitutional subtelomeric 1p36.3 deletion/duplication in a mentally retarded child with neonatal neuroblastoma.
Isidor B, Le Cunff M, Boceno M, Boisseau P, Thomas C, Rival JM, David A, Le Caignec C.
Eur J Med Genet. 2008 Nov-Dec;51(6):679-84. Epub 2008 Jul 11.
PMID 18672103
Mechanisms of CHD5 Inactivation in Neuroblastomas.
Koyama H, Zhuang T, Light JE, Kolla V, Higashi M, McGrady PW, London WB, Brodeur GM.
Clin Cancer Res. 2012 Mar 15;18(6):1588-97. Epub 2012 Jan 31.
PMID 22294723
Preliminary evidence for involvement of the tumour suppressor gene CHD5 in a family with cutaneous melanoma.
Lang J, Tobias ES, Mackie R.
Br J Dermatol. 2011 May;164(5):1010-6. doi: 10.1111/j.1365-2133.2011.10223.x.
PMID 21250965
Molecular cytogenetic analysis of chromosomes 1 and 19 in glioma cell lines.
Law ME, Templeton KL, Kitange G, Smith J, Misra A, Feuerstein BG, Jenkins RB.
Cancer Genet Cytogenet. 2005 Jul 1;160(1):1-14.
PMID 15949564
Distinct high-profile methylated genes in colorectal cancer.
Mokarram P, Kumar K, Brim H, Naghibalhossaini F, Saberi-firoozi M, Nouraie M, Green R, Lee E, Smoot DT, Ashktorab H.
PLoS One. 2009 Sep 11;4(9):e7012.
PMID 19750230
Chromatin remodeling factor CHD5 is silenced by promoter CpG island hypermethylation in human cancer.
Mulero-Navarro S, Esteller M.
Epigenetics. 2008 Jul-Aug;3(4):210-5. Epub 2008 Jul 16.
PMID 18698156
Mutation screening of CHD5 in melanoma-prone families linked to 1p36 revealed no deleterious coding or splice site changes.
Ng D, Yang XR, Tucker MA, Goldstein AM.
BMC Res Notes. 2008 Sep 19;1:86.
PMID 18803848
Expression and sequence analysis of candidates for the 1p36.31 tumor suppressor gene deleted in neuroblastomas.
Okawa ER, Gotoh T, Manne J, Igarashi J, Fujita T, Silverman KA, Xhao H, Mosse YP, White PS, Brodeur GM.
Oncogene. 2008 Jan 31;27(6):803-10. Epub 2007 Jul 30.
PMID 17667943
CHD5, a brain-specific paralog of Mi2 chromatin remodeling enzymes, regulates expression of neuronal genes.
Potts RC, Zhang P, Wurster AL, Precht P, Mughal MR, Wood WH 3rd, Zhang Y, Becker KG, Mattson MP, Pazin MJ.
PLoS One. 2011;6(9):e24515. Epub 2011 Sep 13.
PMID 21931736
Copy number and targeted mutational analysis reveals novel somatic events in metastatic prostate tumors.
Robbins CM, Tembe WA, Baker A, Sinari S, Moses TY, Beckstrom-Sternberg S, Beckstrom-Sternberg J, Barrett M, Long J, Chinnaiyan A, Lowey J, Suh E, Pearson JV, Craig DW, Agus DB, Pienta KJ, Carpten JD.
Genome Res. 2011 Jan;21(1):47-55. Epub 2010 Dec 8.
PMID 21147910
CHD5, a new member of the chromodomain gene family, is preferentially expressed in the nervous system.
Thompson PM, Gotoh T, Kok M, White PS, Brodeur GM.
Oncogene. 2003 Feb 20;22(7):1002-11.
PMID 12592387
The involvement of CHD5 hypermethylation in laryngeal squamous cell carcinoma.
Wang J, Chen H, Fu S, Xu ZM, Sun KL, Fu WN.
Oral Oncol. 2011 Jul;47(7):601-8. Epub 2011 Jun 1.
PMID 21636313
CHD5 is down-regulated through promoter hypermethylation in gastric cancer.
Wang X, Lau KK, So LK, Lam YW.
J Biomed Sci. 2009 Oct 19;16:95.
PMID 19840376
Definition and characterization of a region of 1p36.3 consistently deleted in neuroblastoma.
White PS, Thompson PM, Gotoh T, Okawa ER, Igarashi J, Kok M, Winter C, Gregory SG, Hogarty MD, Maris JM, Brodeur GM.
Oncogene. 2005 Apr 14;24(16):2684-94.
PMID 15829979
CHD5 Downregulation Associated with Poor Prognosis in Epithelial Ovarian Cancer.
Wong RR, Chan LK, Tsang TP, Lee CW, Cheung TH, Yim SF, Siu NS, Lee SN, Yu MY, Chim SS, Wong YF, Chung TK.
Gynecol Obstet Invest. 2011;72(3):203-7. Epub 2011 Aug 23.
PMID 21860208
CHD5, a tumor suppressor that is epigenetically silenced in lung cancer.
Zhao R, Yan Q, Lv J, Huang H, Zheng W, Zhang B, Ma W.
Lung Cancer. 2011 Dec 18. [Epub ahead of print]
PMID 22186629


This paper should be referenced as such :
Kolla, V ; Higashi, M ; Zhuang, T ; Brodeur, GM
CHD5 (chromodomain helicase DNA binding protein 5)
Atlas Genet Cytogenet Oncol Haematol. 2012;16(6):392-395.
Free journal version : [ pdf ]   [ DOI ]
History of this paper:
Brodeur, GM ; White, PS. CHD5 (Chromodomain-helicase-DNA binding protein 5). Atlas Genet Cytogenet Oncol Haematol. 2010;14(10):934-936.

External links


HGNC (Hugo)CHD5   16816
Entrez_Gene (NCBI)CHD5    chromodomain helicase DNA binding protein 5
GeneCards (Weizmann)CHD5
Ensembl hg19 (Hinxton)ENSG00000116254 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000116254 [Gene_View]  ENSG00000116254 [Sequence]  chr1:6101787-6180321 [Contig_View]  CHD5 [Vega]
ICGC DataPortalENSG00000116254
TCGA cBioPortalCHD5
AceView (NCBI)CHD5
Genatlas (Paris)CHD5
SOURCE (Princeton)CHD5
Genetics Home Reference (NIH)CHD5
Genomic and cartography
GoldenPath hg38 (UCSC)CHD5  -     chr1:6101787-6180321 -  1p36.31   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)CHD5  -     1p36.31   [Description]    (hg19-Feb_2009)
GoldenPathCHD5 - 1p36.31 [CytoView hg19]  CHD5 - 1p36.31 [CytoView hg38]
Genome Data Viewer NCBICHD5 [Mapview hg19]  
Gene and transcription
Genbank (Entrez)AB007913 AF425231 AK091386 AK126012 AK127046
RefSeq transcript (Entrez)NM_015557
Consensus coding sequences : CCDS (NCBI)CHD5
Gene ExpressionCHD5 [ NCBI-GEO ]   CHD5 [ EBI - ARRAY_EXPRESS ]   CHD5 [ SEEK ]   CHD5 [ MEM ]
Gene Expression Viewer (FireBrowse)CHD5 [ Firebrowse - Broad ]
GenevisibleExpression of CHD5 in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)26038
GTEX Portal (Tissue expression)CHD5
Human Protein AtlasENSG00000116254-CHD5 [pathology]   [cell]   [tissue]
Protein : pattern, domain, 3D structure
UniProt/SwissProtQ8TDI0   [function]  [subcellular_location]  [family_and_domains]  [pathology_and_biotech]  [ptm_processing]  [expression]  [interaction]
NextProtQ8TDI0  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProQ8TDI0
Catalytic activity : Enzyme3.6.4.12 [ Enzyme-Expasy ] [ IntEnz-EBI ] [ BRENDA ] [ KEGG ]   [ MEROPS ]
Domaine pattern : Prosite (Expaxy)CHROMO_2 (PS50013)    DEAH_ATP_HELICASE (PS00690)    HELICASE_ATP_BIND_1 (PS51192)    HELICASE_CTER (PS51194)    ZF_PHD_1 (PS01359)    ZF_PHD_2 (PS50016)   
Domains : Interpro (EBI)CHD5    CHD_C2    CHD_N    Chromo-like_dom_sf    Chromo/chromo_shadow_dom    Chromo_domain    DNA/RNA_helicase_DEAH_CS    DUF1086    DUF1087    Helicase_ATP-bd    Helicase_C    P-loop_NTPase    SNF2-like_sf    SNF2_N    Zinc_finger_PHD-type_CS    Znf_FYVE_PHD    Znf_PHD    Znf_PHD-finger    Znf_RING/FYVE/PHD   
Domain families : Pfam (Sanger)CHDCT2 (PF08074)    CHDNT (PF08073)    Chromo (PF00385)    DUF1086 (PF06461)    DUF1087 (PF06465)    Helicase_C (PF00271)    PHD (PF00628)    SNF2_N (PF00176)   
Domain families : Pfam (NCBI)pfam08074    pfam08073    pfam00385    pfam06461    pfam06465    pfam00271    pfam00628    pfam00176   
Domain families : Smart (EMBL)CHROMO (SM00298)  DEXDc (SM00487)  DUF1086 (SM01146)  DUF1087 (SM01147)  HELICc (SM00490)  PHD (SM00249)  
Conserved Domain (NCBI)CHD5
PDB Europe6GUU   
Structural Biology KnowledgeBase6GUU   
SCOP (Structural Classification of Proteins)6GUU   
CATH (Classification of proteins structures)6GUU   
AlphaFold pdb e-kbQ8TDI0   
Human Protein Atlas [tissue]ENSG00000116254-CHD5 [tissue]
Protein Interaction databases
IntAct (EBI)Q8TDI0
Ontologies - Pathways
Ontology : AmiGOheterochromatin  DNA binding  DNA helicase activity  ATP binding  nucleus  nucleoplasm  cytosol  regulation of transcription by RNA polymerase II  negative regulation of cell population proliferation  membrane  NuRD complex  nuclear speck  hydrolase activity  cerebral cortex neuron differentiation  DNA duplex unwinding  spermatogenesis, exchange of chromosomal proteins  histone H4 acetylation  metal ion binding  H3K27me3 modified histone binding  nucleosome-dependent ATPase activity  histone H3-K27 trimethylation  positive regulation of signal transduction by p53 class mediator  
Ontology : EGO-EBIheterochromatin  DNA binding  DNA helicase activity  ATP binding  nucleus  nucleoplasm  cytosol  regulation of transcription by RNA polymerase II  negative regulation of cell population proliferation  membrane  NuRD complex  nuclear speck  hydrolase activity  cerebral cortex neuron differentiation  DNA duplex unwinding  spermatogenesis, exchange of chromosomal proteins  histone H4 acetylation  metal ion binding  H3K27me3 modified histone binding  nucleosome-dependent ATPase activity  histone H3-K27 trimethylation  positive regulation of signal transduction by p53 class mediator  
NDEx NetworkCHD5
Atlas of Cancer Signalling NetworkCHD5
Wikipedia pathwaysCHD5
Orthology - Evolution
GeneTree (enSembl)ENSG00000116254
Phylogenetic Trees/Animal Genes : TreeFamCHD5
Homologs : HomoloGeneCHD5
Homology/Alignments : Family Browser (UCSC)CHD5
Gene fusions - Rearrangements
Fusion : QuiverCHD5
Polymorphisms : SNP and Copy number variants
NCBI Variation ViewerCHD5 [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)CHD5
Exome Variant ServerCHD5
GNOMAD BrowserENSG00000116254
Varsome BrowserCHD5
ACMGCHD5 variants
Genomic Variants (DGV)CHD5 [DGVbeta]
DECIPHERCHD5 [patients]   [syndromes]   [variants]   [genes]  
CONAN: Copy Number AnalysisCHD5 
ICGC Data PortalCHD5 
TCGA Data PortalCHD5 
Broad Tumor PortalCHD5
OASIS PortalCHD5 [ Somatic mutations - Copy number]
Somatic Mutations in Cancer : COSMICCHD5  [overview]  [genome browser]  [tissue]  [distribution]  
Somatic Mutations in Cancer : COSMIC3DCHD5
Mutations and Diseases : HGMDCHD5
LOVD (Leiden Open Variation Database)[gene] [transcripts] [variants]
DgiDB (Drug Gene Interaction Database)CHD5
DoCM (Curated mutations)CHD5
CIViC (Clinical Interpretations of Variants in Cancer)CHD5
NCG (London)CHD5
Impact of mutations[PolyPhen2] [Provean] [Buck Institute : MutDB] [Mutation Assessor] [Mutanalyser]
Genetic Testing Registry CHD5
NextProtQ8TDI0 [Medical]
Target ValidationCHD5
Huge Navigator CHD5 [HugePedia]
Clinical trials, drugs, therapy
Protein Interactions : CTDCHD5
Pharm GKB GenePA134969178
Clinical trialCHD5
DataMed IndexCHD5
Other databaseFABLE
PubMed59 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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