SMYD4

SET and MYND domain-containing protein 4 is a protein that in humans is encoded by the SMYD4 gene.[5][6]

SMYD4
Identifiers
Aliases	SMYD4, ZMYND21, SET and MYND domain containing 4
External IDs	MGI: 2442796 HomoloGene: 35098 GeneCards: SMYD4
Gene location (Human) Chr. Chromosome 17 (human)[1] Band 17p13.3 Start 1,779,485 bp[1] End 1,830,634 bp[1]
Gene location (Mouse) Chr. Chromosome 11 (mouse)[2] Band 11|11 B5 Start 75,348,433 bp[2] End 75,405,705 bp[2]
Orthologs
Species	Human	Mouse
Entrez	114826	319822
Ensembl	ENSG00000186532	ENSMUSG00000018809
UniProt	Q8IYR2	Q8BTK5
RefSeq (mRNA)	NM_052928	NM_001102611 NM_177009
RefSeq (protein)	NP_443160	NP_001096081
Location (UCSC)	Chr 17: 1.78 – 1.83 Mb	Chr 11: 75.35 – 75.41 Mb
PubMed search	[3]	[4]
Wikidata
View/Edit Human View/Edit Mouse

Model organisms

Smyd4 knockout mouse phenotype

Characteristic	Phenotype
Homozygote viability	Normal
Body weight	Normal
Anxiety	Normal
Neurological assessment	Normal
Grip strength	Normal
Hot plate	Normal
Dysmorphology	Normal
Indirect calorimetry	Normal
Glucose tolerance test	Normal
Auditory brainstem response	Normal
DEXA	Normal
Radiography	Normal
Body temperature	Normal
Eye morphology	Normal
Clinical chemistry	Normal
Plasma immunoglobulins	Normal
Haematology	Normal
Peripheral blood lymphocytes	Normal
Micronucleus test	Normal
Heart weight	Normal
Tail epidermis wholemount	Normal
Skin Histopathology	Normal
Brain histopathology	Normal
Eye Histopathology	Normal
Salmonella infection	Normal[7]
Citrobacter infection	Normal[8]
All tests and analysis from[9][10]

Model organisms have been used in the study of SMYD4 function. A conditional knockout mouse line, called Smyd4^{tm1a(EUCOMM)Wtsi}[11][12] 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 — at the Wellcome Trust Sanger Institute.[13][14][15]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[9][16] Twenty six tests were carried out on homozygous mutant adult mice, however no significant abnormalities were observed.[9]

References

1. GRCh38: Ensembl release 89: ENSG00000186532 - Ensembl, May 2017
2. GRCm38: Ensembl release 89: ENSMUSG00000018809 - Ensembl, May 2017
3. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
4. "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
5. Nagase T; Kikuno R; Ohara O (Sep 2001). "Prediction of the coding sequences of unidentified human genes. XXI. The complete sequences of 60 new cDNA clones from brain which code for large proteins". DNA Res. 8 (4): 179–87. doi:10.1093/dnares/8.4.179. PMID 11572484.
6. "Entrez Gene: SMYD4 SET and MYND domain containing 4".
7. "Salmonella infection data for Smyd4". Wellcome Trust Sanger Institute.
8. "Citrobacter infection data for Smyd4". Wellcome Trust Sanger Institute.
9. Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica. 88 (S248). doi:10.1111/j.1755-3768.2010.4142.x.
10. Mouse Resources Portal, Wellcome Trust Sanger Institute.
11. "International Knockout Mouse Consortium".
12. "Mouse Genome Informatics".
13. Skarnes, W. C.; Rosen, B.; West, A. P.; Koutsourakis, M.; Bushell, W.; Iyer, V.; Mujica, A. O.; Thomas, M.; Harrow, J.; Cox, T.; Jackson, D.; Severin, J.; Biggs, P.; Fu, J.; Nefedov, M.; De Jong, P. J.; Stewart, A. F.; Bradley, A. (2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–342. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
14. Dolgin E (June 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
15. Collins FS; Rossant J; Wurst W (January 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
16. van der Weyden L; White JK; Adams DJ; Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biol. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.

Further reading

• Kimura K, Wakamatsu A, Suzuki Y, et al. (2006). "Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes". Genome Res. 16 (1): 55–65. doi:10.1101/gr.4039406. PMC 1356129. PMID 16344560.
• Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC)". Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMC 528928. PMID 15489334.
• Brandenberger R, Wei H, Zhang S, et al. (2005). "Transcriptome characterization elucidates signaling networks that control human ES cell growth and differentiation". Nat. Biotechnol. 22 (6): 707–16. doi:10.1038/nbt971. PMID 15146197.
• Ota T, Suzuki Y, Nishikawa T, et al. (2004). "Complete sequencing and characterization of 21,243 full-length human cDNAs". Nat. Genet. 36 (1): 40–5. doi:10.1038/ng1285. PMID 14702039.
• Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932.
• Xu XR, Huang J, Xu ZG, et al. (2002). "Insight into hepatocellular carcinogenesis at transcriptome level by comparing gene expression profiles of hepatocellular carcinoma with those of corresponding noncancerous liver". Proc. Natl. Acad. Sci. U.S.A. 98 (26): 15089–94. doi:10.1073/pnas.241522398. PMC 64988. PMID 11752456.
• Bonaldo MF; Lennon G; Soares MB (1997). "Normalization and subtraction: two approaches to facilitate gene discovery". Genome Res. 6 (9): 791–806. doi:10.1101/gr.6.9.791. PMID 8889548.