KDM4C

Lysine (K)-specific demethylase 4C

Rendering based on PDB 2XDP​.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols KDM4C ; GASC1; JHDM3C; JMJD2C; TDRD14C
External IDs OMIM: 605469 MGI: 1924054 HomoloGene: 41004 ChEMBL: 6175 GeneCards: KDM4C Gene
EC number 1.14.11.-
RNA expression pattern
More reference expression data
Orthologs
Species Human Mouse
Entrez 23081 76804
Ensembl ENSG00000107077 ENSMUSG00000028397
UniProt Q9H3R0 Q8VCD7
RefSeq (mRNA) NM_001146694 NM_001172095
RefSeq (protein) NP_001140167 NP_001165566
Location (UCSC) Chr 9:
6.72 – 7.08 Mb		 Chr 4:
74.24 – 74.41 Mb
PubMed search

Lysine-specific demethylase 4C is an enzyme that in humans is encoded by the KDM4C gene.[1][2][3]

Function

This gene is a member of the Jumonji domain 2 (JMJD2) family and encodes a protein with one JmjC domain, one JmjN domain, two PHD-type zinc fingers, and two Tudor domains. This nuclear protein functions as a trimethylation-specific demethylase, converting specific trimethylated histone residues to the dimethylated form. Chromosomal aberrations and increased transcriptional expression of this gene are associated with esophageal squamous cell carcinoma.[3]

Model organisms

Model organisms have been used in the study of KDM4C function. A conditional knockout mouse line, called Kdm4ctm1a(KOMP)Wtsi[9][10] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[11][12][13]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[7][14] Twenty five tests were carried out on mutant mice and two significant abnormalities were observed.[7] Homozygous mutant males had decreased haematocrit and haemoglobin levels, while animals of both sex displayed an increase in sebaceous gland size.[7]

References

  1. ↑ Nagase T, Ishikawa K, Suyama M, Kikuno R, Miyajima N, Tanaka A, Kotani H, Nomura N, Ohara O (Oct 1998). "Prediction of the coding sequences of unidentified human genes. XI. The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro". DNA Research 5 (5): 277–86. doi:10.1093/dnares/5.5.277. PMID 9872452.
  2. ↑ Katoh M, Katoh M (Jun 2004). "Identification and characterization of JMJD2 family genes in silico". International Journal of Oncology 24 (6): 1623–8. doi:10.3892/ijo.25.3.759. PMID 15138608.
  3. 1 2 "Entrez Gene: JMJD2C jumonji domain containing 2C".
  4. ↑ "Haematology data for Kdm4c". Wellcome Trust Sanger Institute.
  5. ↑ "Salmonella infection data for Kdm4c". Wellcome Trust Sanger Institute.
  6. ↑ "Citrobacter infection data for Kdm4c". Wellcome Trust Sanger Institute.
  7. 1 2 3 4 Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica 88: 925–7. doi:10.1111/j.1755-3768.2010.4142.x.
  8. ↑ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  9. ↑ "International Knockout Mouse Consortium".
  10. ↑ "Mouse Genome Informatics".
  11. ↑ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (Jun 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  12. ↑ Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  13. ↑ Collins FS, Rossant J, Wurst W (Jan 2007). "A mouse for all reasons". Cell 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
  14. ↑ van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biology 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.

Further reading

  • Yang ZQ, Imoto I, Fukuda Y, Pimkhaokham A, Shimada Y, Imamura M, Sugano S, Nakamura Y, Inazawa J (Sep 2000). "Identification of a novel gene, GASC1, within an amplicon at 9p23-24 frequently detected in esophageal cancer cell lines". Cancer Research 60 (17): 4735–9. PMID 10987278. 
  • Kimura K, Wakamatsu A, Suzuki Y, Ota T, Nishikawa T, Yamashita R, Yamamoto J, Sekine M, Tsuritani K, Wakaguri H, Ishii S, Sugiyama T, Saito K, Isono Y, Irie R, Kushida N, Yoneyama T, Otsuka R, Kanda K, Yokoi T, Kondo H, Wagatsuma M, Murakawa K, Ishida S, Ishibashi T, Takahashi-Fujii A, Tanase T, Nagai K, Kikuchi H, Nakai K, Isogai T, Sugano S (Jan 2006). "Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes". Genome Research 16 (1): 55–65. doi:10.1101/gr.4039406. PMC 1356129. PMID 16344560. 
  • Whetstine JR, Nottke A, Lan F, Huarte M, Smolikov S, Chen Z, Spooner E, Li E, Zhang G, Colaiacovo M, Shi Y (May 2006). "Reversal of histone lysine trimethylation by the JMJD2 family of histone demethylases". Cell 125 (3): 467–81. doi:10.1016/j.cell.2006.03.028. PMID 16603238. 
  • Cloos PA, Christensen J, Agger K, Maiolica A, Rappsilber J, Antal T, Hansen KH, Helin K (Jul 2006). "The putative oncogene GASC1 demethylates tri- and dimethylated lysine 9 on histone H3". Nature 442 (7100): 307–11. doi:10.1038/nature04837. PMID 16732293. 
  • Wissmann M, Yin N, Müller JM, Greschik H, Fodor BD, Jenuwein T, Vogler C, Schneider R, Günther T, Buettner R, Metzger E, Schüle R (Mar 2007). "Cooperative demethylation by JMJD2C and LSD1 promotes androgen receptor-dependent gene expression". Nature Cell Biology 9 (3): 347–53. doi:10.1038/ncb1546. PMID 17277772. 
  • Katoh Y, Katoh M (Aug 2007). "Comparative integromics on JMJD2A, JMJD2B and JMJD2C: preferential expression of JMJD2C in undifferentiated ES cells". International Journal of Molecular Medicine 20 (2): 269–73. doi:10.3892/ijmm.20.2.269. PMID 17611647. 
  • Erhu Zhao, Jane Ding,.....Hongjuan Cui, Han-Fei Ding (2016). "KDM4C and ATF4 Cooperate in Transcriptional Control of Amino Acid Metabolism". Cell Reports. doi:10.1016/j.celrep.2015.12.053. 


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