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anti-Human Growth Hormone 1 Antikörper:
anti-Mouse (Murine) Growth Hormone 1 Antikörper:
anti-Rat (Rattus) Growth Hormone 1 Antikörper:
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Human Monoclonal Growth Hormone 1 Primary Antibody für ICC, IF - ABIN268996
Thompson, Seethala, Müller: Ectopic sphenoid sinus pituitary adenoma (ESSPA) with normal anterior pituitary gland: a clinicopathologic and immunophenotypic study of 32 cases with a comprehensive review of the english literature. in Head and neck pathology 2012
Show all 2 Pubmed References
Human Polyclonal Growth Hormone 1 Primary Antibody für - ABIN285499
Staloch, Divine, Witten, Simon: C/EBP and Cdx family factors regulate liver fatty acid binding protein transgene expression in the small intestinal epithelium. in Biochimica et biophysica acta 2005
Human Monoclonal Growth Hormone 1 Primary Antibody für FACS, IF - ABIN5578783
Niall, Hogan, Sauer, Rosenblum, Greenwood: Sequences of pituitary and placental lactogenic and growth hormones: evolution from a primordial peptide by gene reduplication. in Proceedings of the National Academy of Sciences of the United States of America 1971
Significant correlations were observed between GH concentration and impairments on several EDI-2 subscales (drive for thinness, body dissatisfaction, interoceptive awareness, sense of ineffectiveness, interpersonal distrust, maturity fear) and on SCL-90 subitems (depression, hostility, obsessivity compulsivity, anxiety), suggesting a possible hormonal modulatory effect on specific aspects of eating disorders.
Patients examined at 1 year or several years from complicated mild traumatic brain injury had a similarly high occurrence of isolated GH deficiency
Single nucleotide variant in GH1 gene is associated with isolated growth hormone deficiency.
In newborns, serum PRL and hGH levels show a positive correlation that can be explained by common regulatory factors or a drift phenomenon. A higher gestational week is associated with a higher PRL/hGH ratio.
This review describes the endocrine profile of centenarians concerning the GH/IGF-I/insulin system, focusing on the relevance of this pathway on the modulation of ageing and longevity.
Data suggest that patients with NICTH (non-islet cell tumor hypoglycemia) exhibit low serum growth hormone levels during hypoglycemic episodes. [Retrospective Study & REVIEW of Case Reports]
Homozygous GH1 deletion is associated with growth hormone deficiency.
Human Growth Hormone Inhibits CLAUDIN-1 Expression Through Activation of Signal Transducer and Activator of Transcription 3 (STAT3).
Serum GH was unrelated to type 2 diabetes, fasting blood glucose, or HbA1c level.
GH1 and GHRHR screening revealed eleven variations in 24 (21%) patients with isolated growth hormone deficiency of which, four were novel deleterious, one novel non-pathogenic and six reported changes.
The results suggest that GH regulates energy metabolism directly in myocytes and that UCP2 participates in the signal transduction pathway that functions downstream of the GHR/JAK/STAT.
These results implicate TIMP3 as a modulator of cell surface GHR abundance and the ability of GH to promote cellular signaling.
Children with GH excess underwent medical treatment with lanreotide and a minimum clinical/biochemical follow up of 2 years is reported. The present study demonstrates that GH excess should be considered as a relative frequent endocrine manifestation in NF1 patients, similarly to central precocious puberty
Thus, GHRH analogs of the Miami series powerfully suppress tumor growth, but have only a weak endocrine GH inhibitory activity. The suppression of tumor growth could be induced in part by the downregulation of GHRH receptors levels.
the levels and kinetics of phosphorylation mediated by the main signalling proteins triggered by 22K-GH or 20K-GH were not exactly the same.
A negative regulation of locally produced GH by androgens/AR in Prostate cancer cells following treatment with AR agonists (R1881) and antagonists (enzalutamide, bicalutamide).
The intrinsic amyloidogenicity of growth hormone, in the presence of contaminating prion protein (and perhaps prolactin as well) and amyloid-beta contained in some cadavers' pituitaries, may have led to the observed co-occurring of Creutzfeldt-Jakob disease and Alzheimer's disease.
GH potentially negatively modulates the maturation and accumulation of lipid in adipocytes.
To our knowledge, c.-223C>T is the first homozygous point mutation in the GH1 promoter that leads to short stature due to idiopathic growth hormone deficiency.
Data show that the recombinant protein produced by the plasmid-free E coli strain was purified and characterized to be human growth hormone (hGH).
The results indicate that increased circulating GH is associated with a reduced ovarian primordial follicle reserve and increased pFoxO3a content in oocytes.
These results indicate that up-regulation of GH in the lungs of DJ-1 KO mice may enhance the malignancy of B16F10 cells and nodule formation in pulmonary metastasis of melanoma.
Confirmation of the impairment of GH-IGF-1 release in hyperphagic MC4R KO mice suggests a role for insulin in regulating both the release of GH, but also in mediating growth during periods of physiologically suppressed GH-IGF-1 levels
When charged with hypoxia-ischemia, mutant brains with deleted IGF-1 receptor were broadly protected from cell damage, neuroinflammation and cerebral edema.
Thiol-disulfide exchange reactions in hGH and related model peptides were influenced by higher order structure, by the size of the thiol reactant and by an Arg residue adjacent to Cys in the thiol reactant.
Growth hormone deficient mice exhibited renal hypertrophy in tubular epithelial cells.
observations demonstrate that germline loss of ghrelin-O-acyltransferase alters Growth Hormone release and patterning
alter miR-19b concentrations in hematopoietic stem cells (HSCs) and affect HSC migration
Moderate elevations in circulating GH and IGF-I can directly increase basal insulin secretion without impacting beta-cell mass, independent of changes in whole body insulin sensitivity and hyperlipidemia.
Acylated ghrelin is not required for the surge in pituitary growth hormone observed in pregnant mice.
STAT5 signaling is increased in the liver in GH-transgenic mice during the growth period, with a balance between positive and negative effectors resulting in accelerated but controlled growth.
Our data indicate that FGF21 is important in the regulation of beta-cell proliferation and insulin synthesis, probably via modulation of GH signaling
Hepatic GH actions normally serve to inhibit de novo lipogenesis (DNL), where loss of this inhibitory signal may explain, in part, the inappropriate increase in hepatic DNL observed in NAFLD patients.
The effects of osteocalcin on testosterone and on induction of the growth hormone/insulin-like growth factor-1 axis, were investigated.
The development of GH excess induced liver-, kidney-, and pituitary gland-alterations in GH transgenic mice are independent of IGF1 whereas GH- stimulated body growth depends on IGF1.
The role of somatostatin in the expression of growth hormone in male and female mice is reported.
Data suggest that Gh represses H6pd (hexose-6-phosphate dehydrogenase) through locally produced Igf1 (insulin-like growth factor 1); Gh directly represses Hsd11b1 (11-beta-hydroxysteroid dehydrogenase 1) mRNA rather than acting via Igf1 receptor.
GH resistance dramatically exacerbates liver fibrosis in model of inflammatory cholestasis
These results further support a role of GH/IGF-I in regulating mammary tumorigenesis but suggest the ultimate consequences of GH/IGF-I on breast tumor development are dependent on the diet and/or metabolic status.
Exposure of mGH to UV light results in a wide spectrum of chemical modifications with immunogenic consequences.
Tracing Recombinant Bovine Somatotropin Ab(Use) Through Gene Expression in Blood, Hair Follicles, and Milk Somatic Cells.
A microarray analysis showed that lncYYW positively regulates the expression of growth hormone 1 and its downstream genes, AKT1 and PIK3CD, in bovine myoblasts. This discovery provides a good foundation for further study of the mechanism of action of lncYYW during bovine myoblast development
bGH mice had increased body weight and decreased percent fat mass. Serum FGF21 levels were significantly elevated in bGH mice. Expression of Fgf21, Fgfr1, and Klb mRNA in white AT and liver were downregulated or unchanged in bGH mice.
GH/HpaII locus as candidate marker for body weight in cattle rather than MSTN/DraI.
An SNP GH4.1 in a growth hormone gene was significantly related to a weaning weight.
The association of IGF1, GH, and PIT1 markers with growth and reproductive traits were assessed.
Male bovine GH transgenic mice have decreased adiposity, and have increased regulatory T cells and macrophages in mesenteric and subcutaneous white adipose tissue.
The total frequencies for the combined genotypes for the bGH and RORC genes, which provide for superior meat quality and carcass weight, in the populations of Kazakh white-headed cattle
There is an association between a polymorphism in intron 3 of the BGH gene and both body weight at first estrus and first calving.
Whereas only moderate structural changes were observed with up-regulation of GH/IGF-I axis, disruption of the GH receptor had pronounced effects upon tendon ultra-structure.
this study identifies a biochemical mechanism for the regulation of SCFAs on bovine GH and PRL gene transcription in dairy cow anterior pituitary cells
homozygote genotypes of GH (LL) and beta-LG (AA) were superior compared to heterozygote genotypes, whereas, the heterozygote genotype of Pit-1 gene (AB) was desirable
one GH1 SNP, GH33, was significantly associated with milk protein yield in the second lactation. Several GH1 SNPs were significantly associated with fertility.
GH and IGF-I genotypes had no substantial effect on productive parameters, though IGF-I genotype affected calving-first service interval in primiparous cows. However, the genotypes do alter the endocrine/metabolic profiles of the transition dairy cow.
Association of cattle growth hormone gene polymorphism with milk productivity
Leptin modulation of lymphocytic growth hormone plays a role in the regulation of immune response during pregnancy.
Results further demonstrate the multifaceted influences of GH1 on milk production, fertility, and growth-related traits in cattle.
Study of genetic variation in Yakutian cattle (Bos taurus L.) using the prolactin bPRL, growth hormone bGH, and transcription factor bPit-1 genes
More than half of the CSF GHRH pulses observed in the current study were followed by episodes of GH release; leptin suppressed, while neuropeptide Y increased serum GH levels.
Findings suggest that the GH gene polymorphism at codons 127 and 172 was related to body weight, circulating basal GH and insulin, and GHRH-induced GH responses in Japanese Black heifers.
After docking on the nuclear membrane, the porcine growth hormone (GH)-growth hormone receptor (GHR) complex fuses with the nuclear membrane and then enters into the cell nucleus.
Missense mutations within the signal sequence influence the expression and the secretion of GH.
Data indicate that the dual effects of cortistatin on growth hormone release parallel those of somatostatin and are probably mediated by the same receptor(s) and signaling pathway(s) for both peptides.
ghrelin increased growth hormone secretion but not growth hormone synthesis by ovarian follicles
These data demonstrated that feed allowance level has important consequence on embryo survival, embryo development and uterine development, possibly mediated by changes in concentrations of reproductive hormones.
GH deficiency during adolescence has negative effects on learning and memory that emerge by middle-age unless prevented by GH supplementation.
Plasma levels of growth hormone (as well as glucose, insulin, and leptin) are highly correlated with the duration of winter anovulatory phase.
Expression of PRL and GH in the guinea pig is prominent in the anterior pituitary, similar to known expression patterns of PRL and GH for other species.
Reproductive tests showed that double transgenic males did not differ from non-transgenics. It is possible that GHR excess in the muscle tissues of double transgenics may have contributed to lower circulating GH levels and thus reduced the negative effects of this hormone with respect to reproduction.
that concomitant overexpression of GH and GHR resulted in a strong decrease of the somatotrophic axis intracellular signaling by diminishing its principal transcription factor signal transducer and activator of transcription 5.1.
Effects of somatotrophic axis (GH/GHR) double transgenesis on structural and molecular aspects of the zebrafish immune system
The zebrafish gh1 mutant, vizzini, exhibits decreased somatic growth, increased adipose tissue accumulation, and disrupted adipose plasticity after nutrient deprivation.
tbx5 knockdown causes a pseudo GH deficiency in zebrafish during early embryonic stages, and supplementation of exogenous GH can partially restore dysmorphogenesis, apoptosis, cell growth inhibition, and abnormal cardiomyogenesis
Inhibition of GH specific translation did not lead to any discernable morphological changes within 10 days post fertilization.
Findings show similar regulatory growth hormone (GH) and insulin-like growth factor 1 (IGF-1) responses in both Atlantic salmon and rainbow trout.
genetic variation and milk production and composition
This paper contains affinity constants (Ka) and binding capacities (Bmax) calculated according to the method of Scatchard
The protein encoded by this gene is a member of the somatotropin/prolactin family of hormones which play an important role in growth control. The gene, along with four other related genes, is located at the growth hormone locus on chromosome 17 where they are interspersed in the same transcriptional orientation\; an arrangement which is thought to have evolved by a series of gene duplications. The five genes share a remarkably high degree of sequence identity. Alternative splicing generates additional isoforms of each of the five growth hormones, leading to further diversity and potential for specialization. This particular family member is expressed in the pituitary but not in placental tissue as is the case for the other four genes in the growth hormone locus. Mutations in or deletions of the gene lead to growth hormone deficiency and short stature.
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