CHST11

CHST11
Identifiers
Aliases	CHST11, C4ST, C4ST-1, C4ST1, HSA269537, carbohydrate (chondroitin 4) sulfotransferase 11
External IDs	MGI: 1927166 HomoloGene: 56808 GeneCards: CHST11
Genetically Related Diseases
cannabis dependence[1]
Gene ontology Molecular function • transferase activity • sulfotransferase activity • N-acetylgalactosamine 4-O-sulfotransferase activity • N-acetylgalactosamine 4-sulfate 6-O-sulfotransferase activity • chondroitin 4-sulfotransferase activity Cellular component • Golgi apparatus • membrane • Golgi membrane • integral component of membrane Biological process • embryonic skeletal system morphogenesis • chondrocyte development • embryonic digit morphogenesis • negative regulation of apoptotic process • negative regulation of transforming growth factor beta receptor signaling pathway • post-embryonic development • respiratory gaseous exchange • cartilage development • developmental growth • regulation of cell proliferation • embryonic limb morphogenesis • polysaccharide localization • post-anal tail morphogenesis • embryonic viscerocranium morphogenesis • carbohydrate biosynthetic process • chondroitin sulfate biosynthetic process • chondroitin sulfate metabolic process • carbohydrate metabolic process Sources:Amigo / QuickGO
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	50515	58250
Ensembl	ENSG00000171310	ENSMUSG00000034612
UniProt	Q9NPF2	Q9JME2
RefSeq (mRNA)	NM_018413 NM_001173982	NM_021439
RefSeq (protein)	NP_001167453.1 NP_060883.1 NP_060883.1	NP_067414.2
Location (UCSC)	Chr 12: 104.46 – 104.76 Mb	Chr 10: 82.99 – 83.2 Mb
PubMed search	[2]	[3]
Wikidata

View/Edit Human

View/Edit Mouse

Carbohydrate sulfotransferase 11 is an enzyme that in humans is encoded by the CHST11 gene.^[4][5]

Clinical relevance

Mutations in this gene have been associated to susceptibility for osteoarthritis.^[6]

Model organisms

Model organisms have been used in the study of CHST11 function. A conditional knockout mouse line called Chst11^{tm1a(KOMP)Wtsi} was generated at the Wellcome Trust Sanger Institute.^[7] Male and female animals underwent a standardized phenotypic screen^[8] to determine the effects of deletion.^{[9][10][11][12]} Additional screens performed: - In-depth immunological phenotyping^[13] - in-depth bone and cartilage phenotyping^[14]

Chst11 knockout mouse phenotype

Characteristic	Phenotype
All data available at.[8][13][14]
Peripheral blood leukocytes 6 Weeks	Normal
Insulin	Normal
Haematology 6 Weeks	Normal
Homozygous viability at P14	Abnormal
Recessive lethal study	Normal
Body weight	Normal
Neurological assessment	Normal
Grip strength	Normal
Dysmorphology	Normal
Indirect calorimetry	Normal
Glucose tolerance test	Normal
Auditory brainstem response	Normal
DEXA	Normal
Radiography	Normal
Eye morphology	Normal
Clinical chemistry	Normal
Haematology 16 Weeks	Normal
Peripheral blood leukocytes 16 Weeks	Normal
Heart weight	Normal
Salmonella infection	Normal
Cytotoxic T Cell Function	Normal
Spleen Immunophenotyping	Normal
Mesenteric Lymph Node Immunophenotyping	Normal
Bone Marrow Immunophenotyping	Normal
Epidermal Immune Composition	Normal

References

1. "Diseases that are genetically associated with CHST11 view/edit references on wikidata".
2. "Human PubMed Reference:".
3. "Mouse PubMed Reference:".
4. Hiraoka N, Nakagawa H, Ong E, Akama TO, Fukuda MN, Fukuda M (Jun 2000). "Molecular cloning and expression of two distinct human chondroitin 4-O-sulfotransferases that belong to the HNK-1 sulfotransferase gene family". The Journal of Biological Chemistry. 275 (26): 20188–96. doi:10.1074/jbc.M002443200. PMID 10781601.
5. "Entrez Gene: CHST11 carbohydrate (chondroitin 4) sulfotransferase 11".
6. Zeggini E, Panoutsopoulou K, Southam L, Rayner NW, Day-Williams AG, Lopes MC, et al. (Sep 2012). "Identification of new susceptibility loci for osteoarthritis (arcOGEN): a genome-wide association study". Lancet. 380 (9844): 815–23. doi:10.1016/S0140-6736(12)60681-3. PMC 3443899. PMID 22763110.
7. 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. "International Mouse Phenotyping Consortium".
9. 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.
10. Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
11. 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.
12. White JK, Gerdin AK, Karp NA, Ryder E, Buljan M, Bussell JN, Salisbury J, Clare S, Ingham NJ, Podrini C, Houghton R, Estabel J, Bottomley JR, Melvin DG, Sunter D, Adams NC, Tannahill D, Logan DW, Macarthur DG, Flint J, Mahajan VB, Tsang SH, Smyth I, Watt FM, Skarnes WC, Dougan G, Adams DJ, Ramirez-Solis R, Bradley A, Steel KP (Jul 2013). "Genome-wide generation and systematic phenotyping of knockout mice reveals new roles for many genes". Cell. 154 (2): 452–64. doi:10.1016/j.cell.2013.06.022. PMC 3717207. PMID 23870131.
13. "Infection and Immunity Immunophenotyping (3i) Consortium".
14. "OBCD Consortium".

Further reading

• Yamauchi S, Mita S, Matsubara T, Fukuta M, Habuchi H, Kimata K, Habuchi O (Mar 2000). "Molecular cloning and expression of chondroitin 4-sulfotransferase". The Journal of Biological Chemistry. 275 (12): 8975–81. doi:10.1074/jbc.275.12.8975. PMID 10722746.
• Dias Neto E, Correa RG, Verjovski-Almeida S, Briones MR, Nagai MA, da Silva W, Zago MA, Bordin S, Costa FF, Goldman GH, Carvalho AF, Matsukuma A, Baia GS, Simpson DH, Brunstein A, de Oliveira PS, Bucher P, Jongeneel CV, O'Hare MJ, Soares F, Brentani RR, Reis LF, de Souza SJ, Simpson AJ (Mar 2000). "Shotgun sequencing of the human transcriptome with ORF expressed sequence tags". Proceedings of the National Academy of Sciences of the United States of America. 97 (7): 3491–6. doi:10.1073/pnas.97.7.3491. PMC 16267. PMID 10737800.
• Okuda T, Mita S, Yamauchi S, Matsubara T, Yagi F, Yamamori D, Fukuta M, Kuroiwa A, Matsuda Y, Habuchi O (Nov 2000). "Molecular cloning, expression, and chromosomal mapping of human chondroitin 4-sulfotransferase, whose expression pattern in human tissues is different from that of chondroitin 6-sulfotransferase". Journal of Biochemistry. 128 (5): 763–70. doi:10.1093/oxfordjournals.jbchem.a022813. PMID 11056388.
• Mikami T, Mizumoto S, Kago N, Kitagawa H, Sugahara K (Sep 2003). "Specificities of three distinct human chondroitin/dermatan N-acetylgalactosamine 4-O-sulfotransferases demonstrated using partially desulfated dermatan sulfate as an acceptor: implication of differential roles in dermatan sulfate biosynthesis". The Journal of Biological Chemistry. 278 (38): 36115–27. doi:10.1074/jbc.M306044200. PMID 12847091.
• Schmidt HH, Dyomin VG, Palanisamy N, Itoyama T, Nanjangud G, Pirc-Danoewinata H, Haas OA, Chaganti RS (Sep 2004). "Deregulation of the carbohydrate (chondroitin 4) sulfotransferase 11 (CHST11) gene in a B-cell chronic lymphocytic leukemia with a t(12;14)(q23;q32)". Oncogene. 23 (41): 6991–6. doi:10.1038/sj.onc.1207934. PMID 15273723.
• Yamada T, Ohtake S, Sato M, Habuchi O (Dec 2004). "Chondroitin 4-sulphotransferase-1 and chondroitin 6-sulphotransferase-1 are affected differently by uronic acid residues neighbouring the acceptor GalNAc residues". The Biochemical Journal. 384 (Pt 3): 567–75. doi:10.1042/BJ20040965. PMC 1134142. PMID 15324304.
• Yusa A, Kitajima K, Habuchi O (May 2005). "N-linked oligosaccharides are required to produce and stabilize the active form of chondroitin 4-sulphotransferase-1". The Biochemical Journal. 388 (Pt 1): 115–21. doi:10.1042/BJ20041573. PMC 1186699. PMID 15628971.