| |
---|---|
Accession Number: | Q92911 |
Protein Name: | SL55 aka SLC5A5 aka NIS |
Length: | 643 |
Molecular Weight: | 68666.00 |
Species: | Homo sapiens (Human) [9606] |
Number of TMSs: | 13 |
Location1 / Topology2 / Orientation3: | Membrane1 / Multi-pass membrane protein2 |
Substrate | Sodium iodide, Chlorate, Thiocyanate, Selenium cyanide, nitrate, Br-, Tetrafluoroborate, Periodate, Bromate |
Cross database links:
Genevestigator: | Q92911 Q92911 |
---|---|
eggNOG: | prNOG04668 COG0591 |
HEGENOM: | HBG446891 HOG000261662 |
RefSeq: | NP_000444.1 |
Entrez Gene ID: | 6528 |
Pfam: | PF00474 |
OMIM: |
274400 phenotype 601843 gene |
KEGG: | hsa:6528 hsa:6528 |
Gene Ontology
GO:0016021
C:integral to membrane
GO:0005886
C:plasma membrane
GO:0015111
F:iodide transmembrane transporter activity
GO:0006814
P:sodium ion transport
GO:0055085
P:transmembrane transport
GO:0005634
C:nucleus
GO:0008507
F:sodium:iodide symporter activity
GO:0071320
P:cellular response to cAMP
GO:0071371
P:cellular response to gonadotropin stimulus
GO:0006590
P:thyroid hormone generation
| |
References (16)[1] “Cloning of the human sodium iodide symporter.” Smanik P.A.et.al. 8806637 [2] “Increased expression of the Na+/I- symporter in cultured human thyroid cells exposed to thyrotropin and in Graves' thyroid tissue.” Saito T.et.al. 9329364 [3] “The DNA sequence and biology of human chromosome 19.” Grimwood J.et.al. 15057824 [4] “The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).” The MGC Project Teamet.al. 15489334 [5] “Congenital hypothyroidism caused by a mutation in the Na(+)/I(-) symporter.” Fujiwara H.et.al. 9171822 [6] “Novel, missense and loss-of-function mutations in the sodium/iodide symporter gene causing iodide transport defect in three Japanese patients.” Kosugi S.et.al. 9745458 [7] “Congenital hypothyroidism due to mutations in the sodium/iodide symporter: identification of a nonsense mutation producing a downstream cryptic 3' splice site.” Pohlenz J.et.al. 9486973 [8] “A novel mutation in the sodium/iodide symporter gene in the largest family with iodide transport defect.” Kosugi S.et.al. 10487695 [9] “Cloning of the human sodium iodide symporter.” Smanik P.A.et.al. 8806637 [10] “Increased expression of the Na+/I- symporter in cultured human thyroid cells exposed to thyrotropin and in Graves' thyroid tissue.” Saito T.et.al. 9329364 [11] “The DNA sequence and biology of human chromosome 19.” Grimwood J.et.al. 15057824 [12] “The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).” The MGC Project Teamet.al. 15489334 [13] “Congenital hypothyroidism caused by a mutation in the Na(+)/I(-) symporter.” Fujiwara H.et.al. 9171822 [14] “Novel, missense and loss-of-function mutations in the sodium/iodide symporter gene causing iodide transport defect in three Japanese patients.” Kosugi S.et.al. 9745458 [15] “Congenital hypothyroidism due to mutations in the sodium/iodide symporter: identification of a nonsense mutation producing a downstream cryptic 3' splice site.” Pohlenz J.et.al. 9486973 [16] “A novel mutation in the sodium/iodide symporter gene in the largest family with iodide transport defect.” Kosugi S.et.al. 10487695
|
External Searches:
|
Analyze:
Predict TMSs (Predict number of transmembrane segments) | ||||
FASTA formatted sequence |
|
1: MEAVETGERP TFGAWDYGVF ALMLLVSTGI GLWVGLARGG QRSAEDFFTG GRRLAALPVG 61: LSLSASFMSA VQVLGVPSEA YRYGLKFLWM CLGQLLNSVL TALLFMPVFY RLGLTSTYEY 121: LEMRFSRAVR LCGTLQYIVA TMLYTGIVIY APALILNQVT GLDIWASLLS TGIICTFYTA 181: VGGMKAVVWT DVFQVVVMLS GFWVVLARGV MLVGGPRQVL TLAQNHSRIN LMDFNPDPRS 241: RYTFWTFVVG GTLVWLSMYG VNQAQVQRYV ACRTEKQAKL ALLINQVGLF LIVSSAACCG 301: IVMFVFYTDC DPLLLGRISA PDQYMPLLVL DIFEDLPGVP GLFLACAYSG TLSTASTSIN 361: AMAAVTVEDL IKPRLRSLAP RKLVIISKGL SLIYGSACLT VAALSSLLGG GVLQGSFTVM 421: GVISGPLLGA FILGMFLPAC NTPGVLAGLG AGLALSLWVA LGATLYPPSE QTMRVLPSSA 481: ARCVALSVNA SGLLDPALLP ANDSSRAPSS GMDASRPALA DSFYAISYLY YGALGTLTTV 541: LCGALISCLT GPTKRSTLAP GLLWWDLARQ TASVAPKEEV AILDDNLVKG PEELPTGNKK 601: PPGFLPTNED RLFFLGQKEL EGAGSWTPCV GHDGGRDQQE TNL