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Article ; Online: Human growth disorders associated with impaired GH action: Defects in STAT5B and JAK2.

Hwa, Vivian

2020 Volume 519, Page(s) 111063

Abstract: Growth hormone (GH) promotes postnatal human growth primarily by regulating insulin-like growth factor (IGF)-I production through activation of the GH receptor (GHR)-JAK2-signal transducer and activator of transcription (STAT)-5B signaling pathway. ... ...

Abstract	Growth hormone (GH) promotes postnatal human growth primarily by regulating insulin-like growth factor (IGF)-I production through activation of the GH receptor (GHR)-JAK2-signal transducer and activator of transcription (STAT)-5B signaling pathway. Inactivating STAT5B mutations, both autosomal recessive (AR) and dominant-negative (DN), are causal of a spectrum of GH insensitivity (GHI) syndrome, IGF-I deficiency and postnatal growth failure. Only AR STAT5B defects, however, confer additional characteristics of immune dysfunction which can manifest as chronic, potentially fatal, pulmonary disease. Somatic activating STAT5B and JAK2 mutations are associated with a plethora of immune abnormalities but appear not to impact human linear growth. In this review, molecular defects associated with STAT5B deficiency is highlighted and insights towards understanding human growth and immunity is emphasized.
MeSH term(s)	Body Height ; Growth Disorders/immunology ; Growth Disorders/metabolism ; Growth Hormone/metabolism ; Humans ; Janus Kinase 2/metabolism ; STAT5 Transcription Factor/deficiency ; STAT5 Transcription Factor/genetics ; STAT5 Transcription Factor/metabolism
Chemical Substances	STAT5 Transcription Factor ; Growth Hormone (9002-72-6) ; Janus Kinase 2 (EC 2.7.10.2)
Language	English
Publishing date	2020-10-27
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2020.111063
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Article: Human growth disorders associated with impaired GH action: Defects in STAT5B and JAK2

Hwa, Vivian

Molecular and cellular endocrinology. 2021 Jan. 01, v. 519

2021

Abstract	Growth hormone (GH) promotes postnatal human growth primarily by regulating insulin-like growth factor (IGF)-I production through activation of the GH receptor (GHR)-JAK2-signal transducer and activator of transcription (STAT)-5B signaling pathway. Inactivating STAT5B mutations, both autosomal recessive (AR) and dominant-negative (DN), are causal of a spectrum of GH insensitivity (GHI) syndrome, IGF-I deficiency and postnatal growth failure. Only AR STAT5B defects, however, confer additional characteristics of immune dysfunction which can manifest as chronic, potentially fatal, pulmonary disease. Somatic activating STAT5B and JAK2 mutations are associated with a plethora of immune abnormalities but appear not to impact human linear growth. In this review, molecular defects associated with STAT5B deficiency is highlighted and insights towards understanding human growth and immunity is emphasized.
Keywords	human growth ; humans ; immunity ; respiratory tract diseases ; somatotropin ; transactivators
Language	English
Dates of publication	2021-0101
Publishing place	Elsevier B.V.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2020.111063
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: STAT5B deficiency: Impacts on human growth and immunity.

Hwa, Vivian

Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society

2016 Volume 28, Page(s) 16–20

Abstract: Growth hormone (GH) promotes postnatal human growth primarily by regulating insulin-like growth factor (IGF)-I production through activation of the GH receptor (GHR)-signal transducer and activator of transcription (STAT)-5B signaling cascade. The ... ...

Abstract	Growth hormone (GH) promotes postnatal human growth primarily by regulating insulin-like growth factor (IGF)-I production through activation of the GH receptor (GHR)-signal transducer and activator of transcription (STAT)-5B signaling cascade. The critical importance of STAT5B in human IGF-I production was confirmed with the identification of the first homozygous, autosomal recessive, STAT5B mutation in a young female patient who phenotypically resembled patients with classical growth hormone insensitivity (GHI) syndrome (Laron syndrome) due to mutations in the GHR gene, presenting with severe postnatal growth failure and marked IGF-I deficiency. Of note, the closely related STAT5A, which shares >95% amino acid identity with STAT5B, could not compensate for loss of functional STAT5B. To date, 7 homozygous, inactivating, STAT5B mutations in 10 patients have been reported. STAT5B deficient patients, unlike patients deficient in GHR, can also present with a novel, potentially fatal, primary immunodeficiency, which can manifest as chronic pulmonary disease. STAT5B deficiency may be underestimated in endocrine, immunology and pulmonary clinics.
Language	English
Publishing date	2016-06
Publishing country	Scotland
Document type	Journal Article
ZDB-ID	1436781-6
ISSN	1532-2238 ; 1096-6374
ISSN (online)	1532-2238
ISSN	1096-6374
DOI	10.1016/j.ghir.2015.12.006
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Zs.A 3319: Show issues

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Article ; Online: Five-Year Therapy with Recombinant Human Insulin-Like Growth Factor-1 in a Patient with PAPP-A2 Deficiency.

Muthuvel, Gajanthan / Dauber, Andrew / Alexandrou, Eirene / Tyzinski, Leah / Andrew, Melissa / Hwa, Vivian / Backeljauw, Philippe

Hormone research in paediatrics

2023 Volume 96, Issue 5, Page(s) 449–457

Abstract: Introduction: The metalloproteinase pregnancy-associated plasma protein A2 (PAPP-A2) cleaves insulin-like growth factor (IGF)-binding proteins 3 and 5 to release bioactive IGF-I from its ternary complex. Patients with mutations in PAPP-A2 have growth ... ...

Abstract	Introduction: The metalloproteinase pregnancy-associated plasma protein A2 (PAPP-A2) cleaves insulin-like growth factor (IGF)-binding proteins 3 and 5 to release bioactive IGF-I from its ternary complex. Patients with mutations in PAPP-A2 have growth failure and low free IGF-I despite elevated total IGF-I. We describe 5-year treatment response to recombinant human IGF-1 (rhIGF-1) in a patient with PAPP-A2 deficiency, and the phenotype of PAPP-A2 deficiency in three siblings. Methods: Two siblings (P2, P3) with PAPP-A2 deficiency were recruited for rhIGF-1 therapy at 120 μg/kg subcutaneous twice daily, along with a third sibling (P1) for phenotyping. We evaluated efficacy and safety of rhIGF-1 therapy, including effect on metabolic measures and bone mineral density (BMD). Results: Treatment with rhIGF-1 was started in 10.4-year- (P3) and 14.5-year (P2)-old brothers. P2 discontinued therapy due to pseudotumor cerebri. P3 continued rhIGF-1 for 5 years; height velocity increased (3.0 cm/year at baseline; 5.0-7.6 cm/year thereafter) as did height SDS (+0.6). P3's pubertal onset was at 12.4 year. BMD height-adjusted Z-score modestly improved for lumbar spine (+0.4), and decreased in forearm (-0.2) and hip (-0.3). All siblings had hyperinsulinemia. Impaired glucose tolerance (IGT) resolved in P1. P2 showed worsening glucose tolerance (2-h glucose: 225 mg/dL). Impaired fasting glucose and hyperinsulinemia initially resolved for P3, but IGT (2-h glucose: 152 mg/dL) developed during puberty. Conclusion: Therapy with rhIGF-1 modestly improved linear growth in one patient with PAPP-A2 deficiency, but without true catch-up. Therapy was associated with pseudotumor cerebri in a sibling. Initial improvement in BMD and glycemic pattern on rhIGF-1 was not sustained during puberty.
MeSH term(s)	Male ; Humans ; Insulin-Like Growth Factor I/metabolism ; Pseudotumor Cerebri ; Glucose ; Recombinant Proteins/therapeutic use ; Glucose Intolerance ; Hyperinsulinism
Chemical Substances	Insulin-Like Growth Factor I (67763-96-6) ; LY 165163 (8HAJ699EWG) ; Glucose (IY9XDZ35W2) ; Recombinant Proteins
Language	English
Publishing date	2023-01-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2537278-6
ISSN	1663-2826 ; 1663-2818
ISSN (online)	1663-2826
ISSN	1663-2818
DOI	10.1159/000529071
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Article ; Online: Recombinant Human Insulin-Like Growth Factor-1 Treatment of Severe Growth Failure in Three Siblings with STAT5B Deficiency.

Muthuvel, Gajanthan / Al Remeithi, Sareea Salem / Foley, Corinne / Dauber, Andrew / Hwa, Vivian / Backeljauw, Philippe

Hormone research in paediatrics

2023 Volume 97, Issue 2, Page(s) 195–202

Abstract: Introduction: Patients with homozygous recessive mutations in STAT5B have severe progressive postnatal growth failure and insulin-like growth factor-I (IGF-I) deficiency associated with immunodeficiency and increased risk of autoimmune and pulmonary ... ...

Abstract	Introduction: Patients with homozygous recessive mutations in STAT5B have severe progressive postnatal growth failure and insulin-like growth factor-I (IGF-I) deficiency associated with immunodeficiency and increased risk of autoimmune and pulmonary conditions. This report describes the efficacy and safety of recombinant human IGF-1 (rhIGF-1) in treating severe growth failure due to STAT5B deficiency. Case presentation: Three siblings (P1, 4.4 year-old female; P2, 2.3 year-old male; and P3, 7 month-old female) with severe short stature (height SDS [HtSDS] -6.5, -4.9, -5.3, respectively) were referred to the Center for Growth Disorders at Cincinnati Children's Hospital Medical Center. All three had a homozygous mutation (p.Trp631) in STAT5B. Baseline IGF-I was 14.7, 14.1, and 10.8 ng/mL, respectively (all < -2.5 SDS for age and sex), and IGFBP-3 was 796, 603, and 475 ng/mL, respectively (all < -3 SDS for age and sex). The siblings were started on rhIGF-1 at 40 μg/kg/dose twice daily subcutaneously (SQ), gradually increased to 110-120 μg/kg/dose SQ twice daily as tolerated. HtSDS and height velocity (HV) were monitored over time. Results:* Six years of growth data was utilized to quantify growth response in the two older siblings and 5 years of data in the youngest. Pre-treatment HVs were, respectively, 3.0 (P1), 3.0 (P2), and 5.2 (P3) cm/year. With rhIGF-1 therapy, HVs increased to 5.2-6.0, 4.8-7.1, and 5.5-7.4 cm/year, respectively, in the first 3 years of treatment, before they decreased to 4.7, 3.8, and 4.3 cm/year, respectively, at a COVID-19 pandemic delayed follow-up visit and with decreased treatment adherence. ΔHtSDS for P1 and P2 was +2.21 and +0.93, respectively, over 6 years, but -0.62 for P3 after 5 years and in the setting of severe local lipohypertrophy and suboptimal weight gain. P3 also experienced hypoglycemia that limited our ability to maintain target rhIGF-1 dosing. Conclusion: The response to rhIGF-1 therapy is less than observed with rhIGF-1 therapy for patients previously described with severe primary IGF-I deficiency, including patients with documented defects in the growth hormone receptor, but may still provide patients with STAT5B deficiency with an opportunity to prevent worsening growth failure.
MeSH term(s)	Child ; Child, Preschool ; Female ; Humans ; Infant ; Male ; Failure to Thrive ; Growth Disorders ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor I/deficiency ; Insulin-Like Growth Factor I/therapeutic use ; Insulin-Like Peptides ; Recombinant Proteins/therapeutic use ; Siblings ; STAT5 Transcription Factor/genetics ; Syndrome
Chemical Substances	Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor I (67763-96-6) ; Insulin-Like Peptides ; Recombinant Proteins ; STAT5 Transcription Factor ; STAT5B protein, human
Language	English
Publishing date	2023-08-16
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2537278-6
ISSN	1663-2826 ; 1663-2818
ISSN (online)	1663-2826
ISSN	1663-2818
DOI	10.1159/000531491
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Article ; Online: A Novel, Heterozygous, de novo Splicing Variant Affecting the Intracellular Domain of the Growth Hormone Receptor causing a mild short stature.

Giannakopoulos, Aristeidis / Papanastasiou, Anastasios D / Zarkadis, Ioannis K / Andrew, Shayne F / Rosenfeld, Ron G / Efthymiadou, Alexandra / Chrysis, Dionisios / Hwa, Vivian

Hormone research in paediatrics

2023

Abstract: Introduction: Although the majority of Growth Hormone insensitivity syndrome (GHIS) cases are classical, the spectrum of clinical phenotypes has expanded to include "atypical" GHIS subjects with milder phenotypes due to very rare heterozygous growth ... ...

Abstract	Introduction: Although the majority of Growth Hormone insensitivity syndrome (GHIS) cases are classical, the spectrum of clinical phenotypes has expanded to include "atypical" GHIS subjects with milder phenotypes due to very rare heterozygous growth hormone receptor (GHR) mutations with dominant negative effects. Case presentation: A 13-year-old pubertal boy presented with short stature (-1.7 SDS) and delayed bone age (11.5 years). His serum IGF-1 was low (16 ng/ml; reference range: 179-540). IGFBP-3 (1.3 mg/L; 3.1-9.5), and ALS (565 mU/ml; 1500-3500) were also low. GH stimulation test was normal, and GHBP markedly elevated (6300pmol/L; 240-3000). Additionally, the boy had insulin resistance and liver steatosis. His final height reached -1.8 SDS, which was 3.0 SDS below his mid-parental height. GHR gene from genomic DNA and established primary fibroblast culture was analyzed and a synonymous heterozygous GHR: c.945G>A variant, in the last nucleotide of exon 9 (encoding intracellular domain of GHR) was identified. In vitro analysis of the GHR cDNA demonstrated a splicing defect, leading to the heterozygous excision of exon 9. The final predicted product was a truncated GHR protein which explained the elevated GHBP levels. Conclusion: We describe the first synonymous heterozygous GHR splicing variant in exon 9 encoding part of the intracellular domain of GHR identified in a patient with mild short stature, thus supporting the continuum of genotype-phenotype of GHIS.
Language	English
Publishing date	2023-09-19
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2537278-6
ISSN	1663-2826 ; 1663-2818
ISSN (online)	1663-2826
ISSN	1663-2818
DOI	10.1159/000534183
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Article ; Online: Biology of the somatotroph axis (after the pituitary).

Rosenfeld, Ron G / Hwa, Vivian

Annales d'endocrinologie

2017 Volume 78, Issue 2, Page(s) 80–82

Abstract: Normal growth requires that pituitary-secreted growth hormone (GH) bind to its specific receptor and activate a complex signaling cascade, leaving to production of insulin-like growth factor-I (IGF-I), which, in turn, activates its own receptor (IGF1R). ... ...

Abstract	Normal growth requires that pituitary-secreted growth hormone (GH) bind to its specific receptor and activate a complex signaling cascade, leaving to production of insulin-like growth factor-I (IGF-I), which, in turn, activates its own receptor (IGF1R). The GH receptor (GHR) is preformed as a dimer and is transported in a nonligand bound state to the cell surface. Binding of GH to the GHR dimer, results in a conformational change of the dimer, activation of the intracellular Janus Kinase 2 (JAK2) and phosphorylation of signal transducer and activator of transcription (STAT) 5B. Phosphorylated STAT5B dimers are then translocated to the nucleus, where they transcriptionally activate multiple genes, including those for IGF-I, IGF binding protein-3 and the acid-labile subunit (ALS).
MeSH term(s)	Human Growth Hormone/genetics ; Human Growth Hormone/metabolism ; Humans ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/metabolism ; Pituitary Diseases/genetics ; Pituitary Diseases/metabolism ; Receptor, IGF Type 1/genetics ; STAT Transcription Factors/genetics ; Somatotrophs/metabolism ; Somatotrophs/physiology
Chemical Substances	IGF1 protein, human ; STAT Transcription Factors ; Human Growth Hormone (12629-01-5) ; Insulin-Like Growth Factor I (67763-96-6) ; Receptor, IGF Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2017-05-08
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	299-9
ISSN	2213-3941 ; 0003-4266
ISSN (online)	2213-3941
ISSN	0003-4266
DOI	10.1016/j.ando.2017.04.002
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Uh III Zs.132: Show issues

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Article ; Online: Treatment of Short Stature in Aggrecan-deficient Patients With Recombinant Human Growth Hormone: 1-Year Response.

Muthuvel, Gajanthan / Dauber, Andrew / Alexandrou, Eirene / Tyzinski, Leah / Andrew, Melissa / Hwa, Vivian / Backeljauw, Philippe

The Journal of clinical endocrinology and metabolism

2021 Volume 107, Issue 5, Page(s) e2103–e2109

Abstract: Context: Patients with aggrecan (ACAN) deficiency present with dominantly inherited short stature, often with advanced skeletal maturation and premature growth cessation. There is a paucity of information on the effects of growth-promoting interventions. ...

Abstract	Context: Patients with aggrecan (ACAN) deficiency present with dominantly inherited short stature, often with advanced skeletal maturation and premature growth cessation. There is a paucity of information on the effects of growth-promoting interventions. Objective: The aim of this study was to evaluate the efficacy and safety of recombinant human growth hormone (rhGH) therapy on linear growth in children with ACAN deficiency. Methods: Open-label, single-arm, prospective study at Cincinnati Children's Hospital Medical Center. Ten treatment-naïve patients were recruited. Inclusion criteria were a confirmed heterozygous mutation in ACAN, age ≥2 years, prepubertal, bone age (BA) ≥chronological age (CA), and normal insulin-like growth factor I concentration. Treatment was with rhGH (50 µg/kg/day) over 1 year. Main outcomes measured were height velocity (HV) and change in (Δ) height SD score (HtSDS). Results: Ten patients (6 females) were enrolled with median CA of 5.6 years (range 2.4-9.7). Baseline median HtSDS was -2.5 (range -4.3 to -1.1). Median baseline BA was 6.9 years (range 2.5-10.0), with median BA/CA of 1.2 (range 0.9-1.5). Median pretreatment HV was 5.2 cm/year (range 3.8-7.1), increased to 8.3 cm/year (range 7.3-11.2) after 1 year of therapy (P = .004). Median ΔHtSDS after 1 year was +0.62 (range +0.35 to +1.39) (P = .002). Skeletal maturation did not advance inappropriately (median ΔBA/CA -0.1, P = .09). No adverse events related to rhGH were observed. Conclusion: Treatment with rhGH improved linear growth in a cohort of patients with short stature due to ACAN deficiency.
MeSH term(s)	Aggrecans/genetics ; Body Height ; Child ; Child, Preschool ; Dwarfism/drug therapy ; Dwarfism/genetics ; Female ; Human Growth Hormone/adverse effects ; Humans ; Male ; Prospective Studies ; Recombinant Proteins/adverse effects
Chemical Substances	Aggrecans ; Recombinant Proteins ; Human Growth Hormone (12629-01-5)
Language	English
Publishing date	2021-12-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgab904
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Article ; Online: Laron syndrome related to homozygous growth hormone receptor c.784>C mutation in a patient with hypoplastic pulmonary arteries.

Akinci, Ayşehan / Karakurt, Cemşit / Hwa, Vivian / Dündar, Ismail / Çamtosun, Emine

Cardiovascular journal of Africa

2019 Volume 30, Issue 2, Page(s) e7–e8

Abstract: Laron syndrome, also known as growth hormone insensitivity, is an autosomal recessive disorder characterised by short stature due to mutations or deletions in the growth hormone receptor (GHR), leading to congenital insulin-like growth factor 1 (IGF1) ... ...

Abstract	Laron syndrome, also known as growth hormone insensitivity, is an autosomal recessive disorder characterised by short stature due to mutations or deletions in the growth hormone receptor (GHR), leading to congenital insulin-like growth factor 1 (IGF1) deficiency. Cardiac abnormalities, such as patent ductus arteriosus or peripheral vascular disease are rare in patients with Laron syndrome, but cardiac hypertrophy has been observed after IGF1 therapy. In this report, we present a 10-year-and-5-month-old girl with severe peripheral-type pulmonary artery hypoplasia and Laron syndrome related to homozygous GHR c.784>C mutation.
MeSH term(s)	Carrier Proteins/genetics ; Child ; Female ; Genetic Predisposition to Disease ; Homozygote ; Humans ; Laron Syndrome/diagnosis ; Laron Syndrome/genetics ; Mutation ; Phenotype ; Pulmonary Artery/abnormalities ; Pulmonary Artery/diagnostic imaging ; Pulmonary Artery/surgery
Chemical Substances	Carrier Proteins ; somatotropin-binding protein (W06KFL3RDT)
Language	English
Publishing date	2019-01-22
Publishing country	South Africa
Document type	Case Reports
ZDB-ID	2383233-2
ISSN	1680-0745 ; 1996-3467 ; 1015-9657 ; 1995-1892
ISSN (online)	1680-0745 ; 1996-3467
ISSN	1015-9657 ; 1995-1892
DOI	10.5830/CVJA-2019-002
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Zs.A 4813: Show issues

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Article ; Online: Severe growth failure associated with a novel heterozygous nonsense mutation in the GHR transmembrane domain leading to elevated growth hormone binding protein.

Rughani, Ankur / Zhang, Dongsheng / Vairamani, Kanimozhi / Dauber, Andrew / Hwa, Vivian / Krishnan, Sowmya

Clinical endocrinology

2020 Volume 92, Issue 4, Page(s) 331–337

Abstract: Objective: To report a novel mutation in GHR and to characterize a novel mechanism of nonclassical growth hormone insensitivity.: Context: Laron syndrome (LS) is a well-described disorder of growth hormone insensitivity due to mutations in the growth ...

Abstract	Objective: To report a novel mutation in GHR and to characterize a novel mechanism of nonclassical growth hormone insensitivity. Context: Laron syndrome (LS) is a well-described disorder of growth hormone insensitivity due to mutations in the growth hormone receptor (GHR) that leads to short stature. Biochemically, LS patients classically have elevated levels of growth hormone (GH), but low levels of insulin-like growth factor (IGF)-1, IGF binding protein (IGFBP)-3 and GH binding protein (GHBP). Design: Case presentation with in vitro functional studies. Patients: A young male Caucasian child with short stature was found to have growth hormone insensitivity manifested by elevated levels of GH and GHBP. Measurements: Growth hormone stimulation tests revealed baseline GH level of 20.9 µg/L and maximum stimulated GH level of 52.7 µg/L and GHBP level of 4868 pmol/L. GHR gene sequencing revealed a novel heterozygous nonsense mutation (c.800G > A, p.Trp267) in the transmembrane domain of the receptor. Immunoblot analysis of transfected GHR p.Trp267 in HEK293 revealed inhibition of GH-induced STAT5 signalling that was overcome with increasing doses of recombinant human GH. Results: Using an in vitro model, we show that elevated levels of GHBP inhibit the action of GH. Furthermore, our studies demonstrate that this inhibition by GHBP can be overcome by increasing doses of recombinant human GH. Conclusions: To our knowledge, this is the first study to demonstrate in vitro that elevated levels of GHBP attenuate the effect of GH and inhibit GH-induced signalling, thereby leading to short stature. Though this inhibition was overcome in vitro with supraphysiologic doses of GH, significantly above endogenously available GH, it remains to be seen whether such an effect can be replicated in vivo.
MeSH term(s)	Carrier Proteins/genetics ; Child ; Codon, Nonsense/genetics ; Growth Hormone ; HEK293 Cells ; Human Growth Hormone/genetics ; Humans ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/metabolism ; Male ; Receptors, Somatotropin/genetics
Chemical Substances	Carrier Proteins ; Codon, Nonsense ; Receptors, Somatotropin ; Human Growth Hormone (12629-01-5) ; Insulin-Like Growth Factor I (67763-96-6) ; Growth Hormone (9002-72-6) ; somatotropin-binding protein (W06KFL3RDT)
Language	English
Publishing date	2020-01-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	121745-8
ISSN	1365-2265 ; 0300-0664
ISSN (online)	1365-2265
ISSN	0300-0664
DOI	10.1111/cen.14148
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

Order via subito