同: SHBG

同: testosterone-estrogen-binding globulin

同: SHBG

同: SHBG
同: SHBG

WordNet

tell the sex (of young chickens)
the properties that distinguish organisms on the basis of their reproductive roles; "she didnt want to know the sex of the foetus" (同)gender, sexuality
all of the feelings resulting from the urge to gratify sexual impulses; "he wanted a better sex life"; "the film contained no sex or violence" (同)sexual urge
either of the two categories (male or female) into which most organisms are divided; "the war between the sexes"
executed with proper legal authority; "a binding contract"
the protective covering on the front, back, and spine of a book; "the book had a leather binding" (同)book binding, cover, back
strip sewn over or along an edge for reinforcement or decoration
the capacity to attract and hold something
the secretion of an endocrine gland that is transmitted by the blood to the tissue on which it has a specific effect (同)endocrine, internal_secretion
a family of proteins found in blood and milk and muscle and in plant seed
having sexual differentiation
characterized by sexuality; "highly sexed"

PrepTutorEJDIC

〈U〉〈C〉『性』,性別 / 《the~》《形容詞を伴い集合的に》『男性』,『女性』 / 〈U〉(男女(雌雄)間の)相違[の意識] / 〈U〉性に関する事柄(情報) / 〈U〉性交 / 〈ひよこなど〉‘の'性別を見分ける
義務的な,拘束力ある / 〈U〉しばること;〈C〉しばる物 / 〈C〉製本,装丁 / 〈U〉縁(‘ふち')取り材料
ホルモン
グロブリン(動植物組織内の純蛋白(たんぱく)質の総称)

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/05/21 01:41:39」(JST)

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[Wiki en表示]

Sex hormone-binding globulin (SHBG) or sex steroid-binding globulin (SSBG) is a glycoprotein that binds to the sex hormones, androgen and estrogen. Other steroid hormones such as progesterone, cortisol, and other corticosteroids are bound by transcortin. SHBG is found in all vertebrates apart from birds.^[1]

Transport of sex hormones

Testosterone and estradiol circulate in the bloodstream, bound mostly to SHBG and to a lesser extent serum albumin and corticosteroid-binding globulin (CBG) (AKA transcortin). Only a very small fraction of about 1-2% is unbound, or "free," and thus biologically active and able to enter a cell and activate its receptor. SHBG inhibits the function of these hormones. Thus, bioavailability of sex hormones is influenced by the level of SHBG. The relative binding affinity of various sex steroids for SHBG is dihydrotestosterone (DHT) > testosterone > androstenediol > estradiol > estrone.^[2] DHEA is weakly bound to SHBG as well, but DHEA-S is not.^[2] Androstenedione is not bound to SHBG either, and is instead bound solely to albumin.^[3]

SHBG production

SHBG is produced mostly by the liver and is released into the bloodstream. Other sites that produce SHBG include the brain, uterus, testes, and placenta.^[4] Testes-produced SHBG is called androgen-binding protein.

Gene

The gene for SHBG is called Shbg located on chromosome 17^[4] on the short arm between the bands 17p12→p13.^[5] Overlapping on the complimentary DNA strand is the gene for spermidine/spermine N1-acetyltransferase family member 2 (SAT2). Nearby are the genes for p53 and ATP1B2, and fragile X mental retardation, autosomal homolog 2 (FXR2) on the complimentary strand.^[6] There are eight exons, of which exon 1 has three variations called 1L, 1T and 1N which are triggered by three promoters: P_L, P_T and P_N respectively. SHBG comes with the 1L, 2, 3, 4, 5, 6, 7, and 8 exons connected together. A variation includes SHBG-T which is missing exon 7 but with exon 1T promoted by promoter P_T on the opposite strand, which shared with that for SAT2.^[7]

Polymorphisms

There are variations in the genetic material for this protein that have different effects. In humans common polymorphisms include the following:

Rs6259, also called Asp327Asn location 7633209 on Chromosome 17, results in there being an extra N-glycosilation site, and so an extra sugar can be attached. This results in a longer circulation half-life for the protein, and raised levels. A health effect is a lowered risk of endometrial cancer, and another is an increased risk of systemic lupus erythematosus.^[8]

Rs6258 also called Ser156Pro is at position 7631360 on the Chromosome 17.

Rs727428 position 7634474 is in several percent of humans.^[9]

(TAAAA)(n) is five base pairs that repeats a variable number of times on the opposite DNA strand.^[10]

Promoter activation

The mechanism of activating the promoter for SHBG in the liver involves hepatocyte nuclear factor 4 alpha (HNF4A) binding to a DR1 like cis element which then stimulate production. Competing with HNF4A at a third site on the promter is PPARG-2 which reduces copying the gene to RNA. If HNF4A level is low then COUP-TF binds to the fist site and turns off production of SHBG.^[1]

Protein

Sex hormone-binding globulin is homodimeric, meaning it has two identical peptide chains making up its structure. The amino acid sequence is the same as for androgen-binding protein but that has different oligosaccharides attached and is produced in testes.^[4]

SHBG has two two laminin G-like domains which form pockets that bind hydrophobic molecules. The steroids are bound by the LG domain at the amino end of the protein.^[1] Inside the pocket of the domain is a serine residue that attracts the two different types of steroids at different points, thus changing their orientation. Androgens bind at the C3 functiuonal groups on the A ring, and estrogens bind via a hydroxyl attached to C17 on the D ring. The two different orientations change a loop over the entrance to the pocket and the position of trp84 (in humans). Thus the whole protein signals what hormone it carries on its own surface.^[1] The steroid binding LG domain is coded by exons 2 to 5.^[1] A linker region joins the two LG domains together.^[1]

When first produced the SHBG precursor has a leading signal peptide attached with 29 amino acids. The remaining peptide has 373 amino acids.^[11] There are two sulfur bridges.

The sugars are attached at two different N-glycosilation points on apsparagine (351 and 367) and one O-glycosilation (7) point on threonine.^[11]

Metals

A calcium ion is needed to link the two elements of the dimer together. Also a zinc ion is used to orient an otherwise disorganised part of the peptide chain.^[1]

Control

SHBG has both enhancing and inhibiting hormonal influences. It decreases with high levels of insulin, growth hormone, insulin-like growth factor 1 (IGF-1), androgens, prolactin and transcortin. High estrogen, and thyroxine cause it to increase.

In an effort to explain obesity-related reductions in SHBG, recent evidence suggests sugar or monosaccharide-induced hepatic lipogenesis, hepatic lipids in general, and cytokines like TNF-alpha and Interleukin reduce SHBG, whereas insulin does not. As an example anti-psoriatic drugs that inhibit TNF-alpha cause an increase in SHBG. The common downstream mechanism for all of these, including the effect of thyroid hormones^[12] was downregulation of HNF4, hepatocyte nuclear factor 4.^[13]^[14]^[15]^[16]^[17]

Blood values

Reference ranges for blood tests for SHBG have been developed:^[18]

Patient type	Range
Adult female, premenopausal	40 - 120 nmol/L
Adult female, postmenopausal	28 - 112 nmol/L
Adult male	20 - 60 nmol/L
Age 1 - 23 months	60 - 252 nmol/L
Prepubertal (24m - 8y)	72 - 220 nmol/L
Pubertal female	36 - 125 nmol/L
Pubertal male	16 - 100 nmol/L

Conditions associated with high or low levels

SHBG levels are decreased by androgens, administration of anabolic steroids,^[19] polycystic ovary syndrome, hypothyroidism, obesity, Cushing's syndrome, and acromegaly. Low SHBG levels increase the probability of Type 2 Diabetes.^[20] SHBG levels increase with estrogenic states (oral contraceptives), pregnancy, hyperthyroidism, cirrhosis, anorexia nervosa, and certain drugs. Long-term calorie restriction of more than 50 percent increases SHBG, while lowering free and total testosterone and estradiol. DHEA-S, which lacks affinity for SHBG, is not affected by calorie restriction.^[21] Polycystic Ovarian Syndrome is associated with insulin resistance and excess insulin lowers SHBG, which increases free testosterone levels.^[22]

In the womb the human fetus has a low level of SHBG allowing increased activity of sex hormones. After birth, the SHBG level rises and remains at a high level throughout childhood. At puberty the SHBG level halves in girls and goes down to a quarter in boys.^[1] The change at puberty is triggered by growth hormone, and its pulsatility differs in boys and girls. In pregnant women in the last two thirds of pregnancy the SHBG level escalates to five to ten times the usual level for a woman. A hypothesis is that this protects against the effect of hormone produced by the fetus.^[1]

Obese girls are more likely to have an early menarche due to lower levels of SHBG.^[1] Anorexia or a lean physique in women leads to higher SHBG levels, which in turn can lead to amenorrhea.^[1]

Measurement of sex hormones

When checking serum estradiol or testosterone, a total level that includes free and bound fractions can be assayed, or the free portion may be measured alone. A free androgen index expresses the ratio of testosterone to SHBG and can be used to summarize the activity of free testosterone. The best test for testosterone is the bioavailable testosterone. Sex hormone-binding globulin can be measured separate from the total fraction of testosterone.

References

^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k Hammond GL (2011). "Diverse Roles for Sex Hormone-Binding Globulin in Reproduction". Biology of Reproduction 85 (3): 431–441. doi:10.1095/biolreprod.111.092593. ISSN 0006-3363. PMID 21613632.
^ ^a ^b Somboonporn W, Davis SR (June 2004). "Testosterone effects on the breast: implications for testosterone therapy for women". Endocrine Reviews 25 (3): 374–88. doi:10.1210/er.2003-0016. PMID 15180949.
^ Principles and Practice of Endocrinology and Metabolism. Lippincott Williams & Wilkins. 24 April 2001. ISBN 978-0-7817-1750-2. Retrieved 4 August 2012.
^ ^a ^b ^c Hammond GL, Bocchinfuso WP (1996). "Sex hormone-binding globulin: gene organization and structure/function analyses". Horm. Res. 45 (3–5): 197–201. doi:10.1159/000184787. PMID 8964583.
^ *Bérubé D, Séralini GE, Gagné R, Hammond GL (1991). "Localization of the human sex hormone-binding globulin gene (SHBG) to the short arm of chromosome 17 (17p12→p13)". Cytogenetic and Genome Research 54 (1–2): 65–7. doi:10.1159/000132958. PMID 2249477.
^ Joseph DR (1998). "The rat androgen-binding protein (ABP/SHBG) gene contains triplet repeats similar to unstable triplets: evidence that the ABP/SHBG and the fragile X-related 2 genes overlap". Steroids 63 (1): 2–4. doi:10.1016/S0039-128X(97)00087-1. PMID 9437788.
^ Nakhla AM, Hryb DJ, Rosner W, Romas NA, Xiang Z, Kahn SM (2009). "Human sex hormone-binding globulin gene expression- multiple promoters and complex alternative splicing". BMC Molecular Biology 10 (1): 37. doi:10.1186/1471-2199-10-37. ISSN 1471-2199. PMC 2694190. PMID 19416531.
^ Piotrowski P, Gasik R, Lianeri M, Cieślak D, Wudarski M, Hrycaj P, Łacki JK, Jagodziński PP (2009). "Asp327Asn polymorphism of sex hormone-binding globulin gene is associated with systemic lupus erythematosus incidence". Molecular Biology Reports 37 (1): 235–239. doi:10.1007/s11033-009-9639-7. ISSN 0301-4851. PMID 19649728.
^ Svartberg J, Schirmer H, Wilsgaard T, Mathiesen EB, Njølstad I, Løchen ML, Jorde R (2014). "Single-nucleotide polymorphism, rs1799941 in the Sex Hormone-Binding Globulin (SHBG) gene, related to both serum testosterone and SHBG levels and the risk of myocardial infarction, type 2 diabetes, cancer and mortality in men: the Tromsø Study". Andrology 2 (2): 212–218. doi:10.1111/j.2047-2927.2013.00174.x. ISSN 2047-2919. PMID 24327369.
^ Thompson DJ, Healey CS, Baynes C, Kalmyrzaev B, Ahmed S, Dowsett M, Folkerd E, Luben RN, Cox D, Ballinger D, Pharoah PD, Ponder BA, Dunning AM, Easton DF (2008). "Identification of Common Variants in the SHBG Gene Affecting Sex Hormone-Binding Globulin Levels and Breast Cancer Risk in Postmenopausal Women". Cancer Epidemiology Biomarkers & Prevention 17 (12): 3490–3498. doi:10.1158/1055-9965.EPI-08-0734. ISSN 1055-9965. PMC 2660245. PMID 19064566.
^ ^a ^b Hammond, G.L.; D.A. Underhill, C.L. Smith, I.S. Goping, M.J. Harley, N.A. Musto, C.Y. Cheng, C.W. Bardin (1987). "The cDNA-deduced primary structure of human sex hormone-binding globulin and location of its steroid-binding domain". FEBS Letters 215 (1): 100–104. doi:10.1016/0014-5793(87)80121-7. ISSN 0014-5793.
^ Selva DM, Hammond GL (July 2009). "Thyroid hormones act indirectly to increase sex hormone-binding globulin production by liver via hepatocyte nuclear factor-4alpha". J. Mol. Endocrinol. 43 (1): 19–27. doi:10.1677/JME-09-0025. PMID 19336534.
^ "Too much sugar turns off gene that controls the effects of sex steroids". PhysOrg.com. 2007-11-07. Retrieved 2008-02-10.
^ Selva DM, Hogeveen KN, Innis SM, Hammond GL (2007). "Monosaccharide-induced lipogenesis regulates the human hepatic sex hormone–binding globulin gene". J. Clin. Invest. 117 (12): 3979–87. doi:10.1172/JCI32249. PMC 2066187. PMID 17992261.
^ Simó R, Barbosa-Desongles A, Hernandez C, Selva DM (November 2012). "IL1β down-regulation of sex hormone-binding globulin production by decreasing HNF-4α via MEK-1/2 and JNK MAPK pathways". Mol. Endocrinol. 26 (11): 1917–27. doi:10.1210/me.2012-1152. PMID 22902540.
^ Simó R, Barbosa-Desongles A, Lecube A, Hernandez C, Selva DM (February 2012). "Potential role of tumor necrosis factor-α in downregulating sex hormone-binding globulin". Diabetes 61 (2): 372–82. doi:10.2337/db11-0727. PMC 3266423. PMID 22210320.
^ Goto A, Morita A, Goto M, Sasaki S, Miyachi M, Aiba N, Terauchi Y, Noda M, Watanabe S (2012). "Associations of sex hormone-binding globulin and testosterone with diabetes among men and women (the Saku Diabetes study): a case control study". Cardiovasc Diabetol 11: 130. doi:10.1186/1475-2840-11-130. PMC 3537568. PMID 23066943.
^ Unit Code 91215 at Mayo Clinic Medical Laboratories. Retrieved April 2011
^ Ruokonen A, Alén M, Bolton N, Vihko R (July 1985). "Response of serum testosterone and its precursor steroids, SHBG and CBG to anabolic steroid and testosterone self-administration in man". Journal of Steroid Biochemistry 23 (1): 33–8. doi:10.1016/0022-4731(85)90257-2. PMID 3160892.
^ Ding EL, Song Y, Manson JE, Hunter DJ, Lee CC, Rifai N, Buring JE, Gaziano JM, Liu S (2009). "Sex Hormone–Binding Globulin and Risk of Type 2 Diabetes in Women and Men". New England Journal of Medicine 361 (12): 1152–1163. doi:10.1056/NEJMoa0804381. ISSN 0028-4793. PMC 2774225. PMID 19657112.
^ Cangemi R, Friedmann AJ, Holloszy JO, Fontana L (April 2010). "Long-term effects of calorie restriction on serum sex-hormone concentrations in men". Aging Cell 9 (2): 236–42. doi:10.1111/j.1474-9726.2010.00553.x. PMC 3569090. PMID 20096034.
^ Manni A, Pardridge WM, Cefalu W, et al: Bioavailability of albumin-bound testosterone. J Clin Endocrinol Metab 1985;61:705

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 高齢男性におけるテストステロン欠乏症の概要 overview of testosterone deficiency in older men
2. 思春期における多嚢胞性卵巣症候群の診断的評価 diagnostic evaluation of polycystic ovary syndrome in adolescents
3. 性腺機能低下を呈する男性の臨床的特徴および診断 clinical features and diagnosis of male hypogonadism
4. 男性生殖生理学 male reproductive physiology
5. 女性化乳房の疫学、病態生理、および原因 epidemiology pathophysiology and causes of gynecomastia

English Journal

Premenopausal serum sex hormone levels in relation to breast cancer risk, overall and by hormone receptor status-Results from the EPIC cohort.

Kaaks R1, Tikk K, Sookthai D, Schock H, Johnson T, Tjønneland A, Olsen A, Overvad K, Clavel-Chapelon F, Dossus L, Baglietto L, Rinaldi S, Chajes V, Romieu I, Boeing H, Schütze M, Trichopoulou A, Lagiou P, Trichopoulos D, Palli D, Sieri S, Tumino R, Ricceri F, Mattiello A, Buckland G, Ramón Quirós J, Sánchez MJ, Amiano P, Chirlaque MD, Barricarte A, Bas Bueno-de-Mesquita H, van Gils CH, Peeters PH, Andersson A, Sund M, Weiderpass E, Khaw KT, Wareham N, Key TJ, Travis RC, Merritt MA, Gunter MJ, Riboli E, Lukanova A.Author information 1Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.AbstractResults from prospective studies on premenopausal serum hormone levels in relation to breast cancer risk have been inconclusive, especially with regard to tumor subtypes. Using a case-control study nested within the prospective European Prospective Investigation into Cancer and Nutrition (EPIC) cohort (801 breast cancer cases and 1,132 matched control subjects), we analyzed the relationships of prediagnostic serum estradiol, free estradiol, progesterone, testosterone, free testosterone and sex hormone-binding globulin (SHBG) levels with the risk of breast cancer by estrogen and progesterone receptor-positive and -negative breast tumors and by age at diagnoses. Higher prediagnostic serum levels of testosterone and free testosterone were associated with an increased overall risk of breast cancer [ORQ4-Q1 = 1.56 (95% CI 1.15-2.13), ptrend = 0.02 for testosterone and ORQ4-Q1 = 1.33 (95% CI 0.99-1.79), ptrend = 0.04 for free testosterone], but no significant risk association was observed for estradiol, free estradiol, progesterone and SHBG. Tests for heterogeneity between receptor-positive and -negative tumors were not significant. When analysis were stratified by age at tumor diagnosis, the odds ratios observed for estradiol were stronger and borderline significant for breast cancer diagnosed at age less than 50 [ORQ4-Q1 = 1.32 (95% CI 0.87-2.01), ptrend = 0.05] compared to breast cancer diagnosed at age 50 or above [ORQ4-Q1 = 0.94 (95% CI 0.60-1.47), ptrend = 0.34, phet = 0.04]. In conclusion, our data indicate that higher premenopausal circulating testosterone levels are associated with an increased risk of developing breast cancer, but do not show a significant association of estradiol or progesterone with breast cancer risk, overall, by menstrual cycle phase or by tumor receptor status, although a possible risk increase with higher estradiol levels for tumors diagnosed before age 50 was seen.
International journal of cancer. Journal international du cancer.Int J Cancer.2014 Apr 15;134(8):1947-57. doi: 10.1002/ijc.28528. Epub 2013 Oct 24.
Results from prospective studies on premenopausal serum hormone levels in relation to breast cancer risk have been inconclusive, especially with regard to tumor subtypes. Using a case-control study nested within the prospective European Prospective Investigation into Cancer and Nutrition (EPIC) coho
PMID 24155248

Endogenous sex hormones, metabolic syndrome, and diabetes in men and women.

Kim C1, Halter JB.Author information 1Department of Medicine, University of Michigan, 2800 Plymouth Road, Building 16, Room 430 W, Ann Arbor, MI, 48109, USA, cathkim@umich.edu.AbstractEndogenous sex hormones predict impairments of glucose regulation. Cross-sectional studies suggest that lower levels of testosterone in men and higher levels in women increase risk of metabolic syndrome and diabetes, whereas lower levels of sex hormone binding globulin in both men and women increase risk of metabolic syndrome and diabetes. In a systematic review, we summarize existing longitudinal studies, which suggest similar patterns. However, these studies are often limited to a single sex steroid measure. Whether these associations are primarily a marker of adiposity, and whether these associations differ between younger eugonadal vs older hypogonadal adults is also uncertain. The impact of exogenous sex steroid therapy may not reflect relationships between sex hormones and impaired glucose regulation that occur without supplementation. Therefore, examination of endogenous sex steroid trajectories and obesity trajectories within individuals might aid our understanding of how sex steroids contribute to glucose regulation.
Current cardiology reports.Curr Cardiol Rep.2014 Apr;16(4):467. doi: 10.1007/s11886-014-0467-6.
Endogenous sex hormones predict impairments of glucose regulation. Cross-sectional studies suggest that lower levels of testosterone in men and higher levels in women increase risk of metabolic syndrome and diabetes, whereas lower levels of sex hormone binding globulin in both men and women increase
PMID 24585109

Hypoxia disrupts gene modulation along the brain-pituitary-gonad (BPG)-liver axis.

Lu X1, Yu RM2, Murphy MB1, Lau K3, Wu RS4.Author information 1Department of Biology and Chemistry, City University of Hong Kong, 83 Tat Chee Avenue, Kowloon, Hong Kong SAR, China.2School of Environmental and Life Sciences, The University of Newcastle, NSW, Australia.3School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Hong Kong SAR, China.4School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Hong Kong SAR, China. Electronic address: rudolfwu@hku.hk.AbstractHypoxia alters sex hormone concentrations leading to reproductive impairment in fish; however the mechanisms underlying these effects remain largely unknown. Using zebrafish (Danio rerio), this study is the first to demonstrate that hypoxia causes endocrine disruption by simultaneously acting on multiple targets along the brain-pituitary-gonadal (BPG)-liver axis in fish. Alterations in the expression of key genes associated with reproductive endocrine pathways in the brain (sGnRH), pituitary (FSHβ and LHβ), gonads (FSH-R, LH-R, HMGR, StAR, CYP19A, CYP11A, CYP11β and 20β-HSD), and liver were correlated with significant reductions of estradiol in females and testosterone in males. Hypoxia also induced sex-specific and tissue-specific changes in the expression of estrogen, androgen, and membrane progestin receptors along the BPG axis, suggesting disruption of the feedback and synchronization of hormone signals. Furthermore, the hypoxia-induced upregulation of hepatic sex hormone-binding globulin suggests an increase in hormone transport and reduced bioavailability in blood, while upregulation of hepatic CYP3A65 and CYP1A in females suggests an increase in estrogen biotransformation and clearance. Given that the regulation of reproductive hormones and the BPG-liver axis are highly conserved, this study provides new insights into the hypoxia-induced endocrine disrupting mechanisms and reproductive impairment in other vertebrates.
Ecotoxicology and environmental safety.Ecotoxicol Environ Saf.2014 Apr;102:70-8. doi: 10.1016/j.ecoenv.2014.01.017. Epub 2014 Feb 1.
Hypoxia alters sex hormone concentrations leading to reproductive impairment in fish; however the mechanisms underlying these effects remain largely unknown. Using zebrafish (Danio rerio), this study is the first to demonstrate that hypoxia causes endocrine disruption by simultaneously acting on mul
PMID 24580824

Japanese Journal

Leptin is an independent determinant of bone mineral density in men with type 2 diabetes mellitus.

Vasilkova Olga,Mokhort Tatiana,Sharshakova Tamara,Hayashida Naomi,Takamura Noboru
Acta Diabetologica 48(4), 291-295, 2011-12
… Hemoglobin A(1c), immune-reactive insulin (IRI), serum total testosterone, and sex hormone-binding globulin were also evaluated. …
NAID 120003751816

Plasma testosterone and sex hormone-binding globulin concentrations and the risk of prostate cancer among Japanese men : A nested case-control study

SAWADA Norie,IWASAKI Motoki,INOUE Manami,SASAZUKI Shizuka,YAMAJI Taiki,SHIMAZU Taichi,Shoichiro Tsugane for the Japan Public Health Center-based Prospective Study Group
Cancer science 101(12), 2652-2657, 2010-12-10
NAID 10027834956

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★リンクテーブル★

リンク元	「性ホルモン結合グロブリン」「SHBG」「testosterone-estrogen-binding globulin」
関連記事	「binding」「sex」「sex hormone」「globuli」

「性ホルモン結合グロブリン」

Sex hormone-binding globulin
Available structures
PDB	Ortholog search: PDBe, RCSB
List of PDB id codes
	1D2S, 1F5F, 1KDK, 1KDM, 1LHN, 1LHO, 1LHU, 1LHV, 1LHW
Identifiers
Symbols	SHBG ; ABP; SBP; TEBG
External IDs	OMIM: 182205 MGI: 98295 HomoloGene: 813 ChEMBL: 3305 GeneCards: SHBG Gene
Gene ontology
Molecular function	• androgen binding;
Cellular component	• extracellular region; • extracellular vesicular exosome;
Biological process	• primary spermatocyte growth;
	Sources: Amigo / QuickGO
RNA expression pattern
	More reference expression data
Orthologs
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