GHRF (Growth Hormone Releasing Factor) Antibody
- Known as:
- GHRF (Growth Hormone Releasing Factor) Antibody
- Catalog number:
- 22938
- Product Quantity:
- 100 µL
- Category:
- Antibodies
- Supplier:
- Immunostar
- Gene target:
- GHRF (Growth Hormone Releasing Factor) Antibody
Related genes to: GHRF (Growth Hormone Releasing Factor) Antibody
- Gene:
- GHRH NIH gene
- Name:
- growth hormone releasing hormone
- Previous symbol:
- GHRF
- Synonyms:
- -
- Chromosome:
- 20q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: GHRF (Growth Hormone Releasing Factor) Antibody
Related articles to: GHRF (Growth Hormone Releasing Factor) Antibody
- Growth hormone-releasing hormone (GHRH) has shown therapeutic potential in the treatment of various diseases. However, the clinical translation of GHRH receptor (GHRH-R) agonists has been hampered by the short half-life and suboptimal activity. Herein, we report a series of hybrid GHRH analogs developed using sulfono-γ-AA peptide-based peptidomimetic optimization. These hybrid peptides exhibit significantly enhanced potency in activating GHRH-R and stimulating growth hormone release while demonstrating markedly improved serum stability ( > 24 h). Subcutaneous administration of selected peptides in mice with ischemic hindlimb enhanced blood perfusion and preservation of limb function. They also promoted endothelial regeneration and collateral vessel formation, enhancing vascular remodeling and tissue repair. In vitro, the peptides enhanced the angiogenic potential of endothelial cells, primarily through activation of the ERK signaling pathway. Our findings lay a strong foundation for the development of long-acting GHRH-R agonists with promising therapeutic potential for the treatment of vascular and regenerative disease. - Source: PubMed
Publication date: 2026/04/13
Shao HaodongWu YulingMao MengyuNiu XiaokeZhang ChiChen MengGuo ZhitaoLuo JiayanSu XingWang BoYu HongTeng Peng - Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) accumulation, tau hyperphosphorylation, neuroinflammation, and synaptic loss. Existing therapies provide only modest symptomatic relief and fail to slow disease progression. Beyond its role in promoting pituitary growth hormone (GH) secretion, growth hormone-releasing hormone (GHRH) has shown neuroprotective effects in experimental ischemic stroke and spinal muscular atrophy. Here, we explored the therapeutic potential of GHRH and its agonist MR-409 in AD models. In vitro, GHRH(1-44)NH₂ promoted survival, proliferation, and neuronal differentiation of rat hippocampal neural stem cells (NSCs) and human SH-SY5Y neuroblastoma cells under growth factor deprivation and amyloid beta (Aβ) exposure. These effects involved the cAMP/PKA/CREB, ERK1/2, and PI3K/Akt signaling pathways. GHRH also attenuated Aβ-induced neurotoxicity by reducing apoptosis, suppressing GSK-3β activity and tau phosphorylation, restoring nuclear β-catenin, and inhibiting NF-κB-mediated inflammation. In vivo, subcutaneous administration of MR-409 in 5xFAD mice reduced Aβ deposition, tau phosphorylation, gliosis, and proinflammatory cytokine expression. In addition, MR-409 mitigated neuronal and synaptic loss, activated survival and neurogenic pathways, and improved cognitive performance, without altering systemic GH and IGF1 levels. MR-409 also elevated NRF2 mRNA expression while reducing its negative regulator KEAP1. Overall, these findings indicate that GHRH and its analog MR-409 exert neuroprotective effects by modulating key pathological features of AD, including neurodegeneration, impaired neurogenesis, neuroinflammation, and oxidative stress. Given their ability to modulate multiple pathological pathways, GHRH agonists may represent promising therapeutic candidates for AD and other neurodegenerative disorders. - Source: PubMed
Publication date: 2026/04/07
Pedrolli FrancescaMorello GiuliaGesmundo IacopoBanfi DanaFerro AlmaWangpaichitr MedhiSha WeiTamagno ElenaSchally Andrew VGuglielmotto MichelaGranata Riccarda - Acromegaly is a chronic disorder caused by sustained excess of growth hormone (GH) and insulin-like growth factor-1 (IGF-1), most commonly due to GH-secreting pituitary neuroendocrine tumors (PitNETs), mainly limited to Pit-1 expressing lineages. Histopathology remains central to diagnosis, prognosis, and treatment planning. Among GH-secreting or somatotroph neoplasms, densely and sparsely granulated are the most relevant clinicopathological subgroups, as they show distinct morphological, radiological, and clinical profiles. Risk assessment is refined by combining routine histology with immunohistochemistry (IHC), including lineage factors, proliferative markers, and somatostatin receptor (SSTR) subtypes, as well as selected molecular tests. Some assays, such as standardized evaluation of SSTR expression, still require further validation. Radiological signs of invasion complement tissue findings and contribute to practical grading systems. Optimal care requires a multidisciplinary approach that integrates endocrine evaluation, high-quality MRI, and expert neuropathology, essential not only for routine care but also for recognizing atypical presentations of acromegaly, such as pituitary hyperplasia, or ectopic growth hormone-releasing hormone (GHRH) or GH secretion. The integration of clinical, pathological, and molecular information provides the foundation for accurate diagnosis and personalized therapy in acromegaly. - Source: PubMed
Publication date: 2025/11/13
Caballero Gabriela ARibalta TeresaAldecoa Iban - Growth hormone (GH) plays an essential role in the regulation of postnatal growth and metabolism through both direct and GH-IGF-1 axis-mediated mechanisms. GH action involves a complex interplay of endocrine, paracrine and autocrine signals that affect multiple tissues and organs. This review addresses the molecular and physiological fundamentals of GH secretion and action, as well as the multiple factors that modulate it, including central and peripheral signals, metabolic variables, physiological and pharmacological states. The relevance of GH receptor signaling and intracellular pathways involved in tissue response is discussed, as well as the mechanisms of hormone resistance that may arise in different clinical contexts. GH secretion, which is pulsatile, is subject to strict regulation by the hypothalamic-pituitary system, involving GHRH, somatostatin and ghrelin, together with negative feedback from GH and IGF-1. In addition, factors such as sleep, nutrition, stress, age or sex contribute significantly to its physiological variability. The implications of the somatotropic axis in pathological conditions such as GH deficiency, acromegaly or GH insensitivity syndromes are also explored. - Source: PubMed
Publication date: 2026/01/20
Iglesias PedroGuerrero-Pérez Fernando - Growth hormone (GH) is an ancestral hormone secreted from the anterior pituitary gland. In adulthood, it is essential to regulate metabolism. GH synthesis and secretion are regulated in a complex manner, primarily through the actions of hypothalamic neuropeptides (GHRH and somatostatin) that integrate hormonal, metabolic, and neurogenic signals. Currently, recombinant human GH is widely used to treat growth hormone deficiency (GHD) and numerous non-GHD disorders, such as short stature and catabolic conditions. Conversely, an excess of GH may lead to different and severe conditions, such as acromegaly, gigantism, Carney complex, McCune-Albright syndrome, neurofibromatosis, and multiple endocrine neoplasia type 1. In patients with growth hormone excess disorders or those treated with GH, skin manifestations are common and can include skin thickening, coarsened facial features, skin tags, oily skin, and excessive sweating. These dermatological changes result from the direct actions of GH and IGF-1 (insulin-like growth factor 1) on skin cells and appendages, leading to increased collagen synthesis and connective tissue expansion. This review focuses on the various skin symptoms associated with these disorders caused by GH excess. This narrative review summarizes recent findings on the management of skin lesions in GH-treated patients and in those with GH excess, highlighting the benefits, side effects, and limitations of current therapies. - Source: PubMed
Publication date: 2026/03/12
Matwiejuk MateuszMyśliwiec HannaMiklosz AgnieszkaChabowski AdrianFlisiak Iwona