GHRF, Rat
- Known as:
- GHRF, Rat
- Catalog number:
- SP-54418-1
- Product Quantity:
- 0.5 mg
- Category:
- -
- Supplier:
- Alpha Dia
- Gene target:
- GHRF Rat
Related genes to: GHRF, Rat
- 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, Rat
α - Calcitonin Gene Related Peptide, α - CGRP, rat'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala13)-Apelin-13 (human, bovine, mouse, rat) 98% C63H107N23O16S CAS: 568565-11-7(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala96)-Myelin Basic Protein (87-99) (human, bovine, rat) 98% C70H110N20O17 CAS:(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2 Related articles to: GHRF, Rat
- Growth hormone-releasing hormone (GHRH) is a hypothalamic neuropeptide that stimulates growth hormone (GH) secretion from the pituitary gland, forming the central GHRH-GH-insulin-like growth factor-1 (IGF-1) endocrine axis. Beyond its classical endocrine function, GHRH and its receptors are widely expressed in extrapituitary tissues, where they regulate diverse physiological processes including cardiovascular function and neuroprotection. Preclinical studies demonstrate that synthetic GHRH analogues like MR-409 mitigate vascular calcification in diabetes, enhance cardiac repair post-myocardial infarction, and restore diastolic function in heart failure through calcium-handling modulation. In ischemic stroke models, MR-409 exhibits neuroprotective effects, reducing mortality and promoting neural regeneration. Studies performed in animal models have demonstrated the efficacy and therapeutic benefits of these compounds in diverse cardiomyopathies and ischemic stroke. Notably, these benefits occur independently of GH/IGF-1 signaling, highlighting their therapeutic potential for cardiovascular and cerebrovascular diseases. This narrative review synthesizes evidence from animal models, underscoring GHRH analogues as promising candidates for clinical translation. The articles included were identified through systematic searches in PubMed using keywords such as "GHRH analogues", "cardiovascular disease', and "ischemic stroke", with selection based on relevance to therapeutic applications and preclinical efficacy. - Source: PubMed
Publication date: 2026/05/28
Ren Hao-LinZhang YuliangYang KefanZhang LuLiu YueyangZhou Ming-Sheng - The arcuate nucleus (ARC) and ventromedial hypothalamus (VMH) are highly specialized hypothalamic nuclei controlling appetite and energy expenditure. Here, we demonstrate that human VMH and ARC neurons can be generated from pluripotent stem cells by fine-tuned timing and duration of bone morphogenetic protein (BMP) exposure. We identified SHH/NKX2.1/FGF10/RAX/TBX3 posterior tuberal progenitors as the source of ARC cell types, including agouti-related peptide (AGRP)-, prepronociceptin (PNOC)-, growth-hormone-releasing hormone (GHRH)-, and thyrotropin-releasing hormone (TRH)-expressing neurons and β2-tanycytes. Differentiated ARC cultures showed high transcriptomic similarity to human ARC and responded to energy homeostasis-regulatory peptides including leptin, glucagon-like peptide 1 (GLP-1), ghrelin, and fibroblast growth factor 1 (FGF1). In contrast, anterior tuberal TBX3 progenitors generated VMH-associated neurons expressing NR5A1, SOX14, and GPR149. Strikingly, two transcriptionally distinct pro-opiomelanocortin (POMC) subpopulations emerged from these lineages, mapping spatially to either the ARC (POMC/TBX3/NR5A2) or the VMH (POMC/SOX14/NR5A1). This model provides a cellular platform to study human hypothalamic subtype specification and pathways involved in central appetite regulation. - Source: PubMed
Publication date: 2026/06/08
Abay-Nørgaard ZehraMueller Anika KHänninen ErnoRausch DylanPiilgaard LouiseTrujillo Lucía SenaFedrizzi LorenzoChristensen Jens BagerSalvador AlisonSchörling Alrik LMottelson Noah WulffQin QiuyuSampath ShruthiHersbach BobHenkenjohann JonasPeeters SofieNikulina ViktoriiaKruse Charlotte HøyLi YuanChinnaiya KavithaPlaczek MarysiaKajtez JankoPers Tune HKirkeby Agnete - Growth hormone deficiency (GHD) is a rare endocrine disorder responsible for growth failure. In the absence of an identified secondary cause, a genetic etiology can be identified, affecting genes involved in hypothalamo-pituitary growth hormone (GH) regulation or in pituitary development itself. The anterior pituitary gland arises from the oral ectoderm and is regulated by neuroectodermal signaling and transcription factors that ensure proper differentiation of hormone-producing cells. GH secretion is stimulated by growth-hormone-releasing hormone (GHRH) and ghrelin, with mutations in their respective receptors (GHRHR, GHSR) contributing to isolated GHD (IGHD). Mutations in GH1, encoding GH itself, are the main genetic cause of IGHD. GHD can also arise from mutations in transcription factor genes such as POU1F1, PROP1, IGSF1 or TBX19 or in genes involved in early brain development such as GLI2, LHX3 or HESX1, potentially leading to syndromic presentations with multi-organ involvement. Understanding the genetic basis of GHD is essential to improving diagnostic strategies, genetic counseling and the development of targeted therapies. Although animal models have been fundamental for understanding pituitary ontogenesis, emerging tools such as human pituitary organoids now offer the promise of dissecting human-specific regulatory mechanisms that cannot be fully captured in traditional animal models. This review aims to provide a comprehensive overview of all known genetic causes of GHD, with a particular focus on the underlying molecular mechanisms and their associated phenotypes. - Source: PubMed
Publication date: 2026/06/05
Aouchiche KarineReynaud RachelCharnay TheoCastinetti FrédéricBrue ThierrySaveanu AlexandruBarlier Anne - The hypothalamic-pituitary-somatotropic (HPS) axis, which includes growth hormone (GH) and insulin-like growth factor 1 (IGF-1), is one of three endocrine systems that show a decline in hormone concentration with age. Among the hypothalamic hormones involved in the aging process, GH-releasing hormone (GHRH) and somatostatin (SST) are most affected, resulting in several age-related changes. The pathophysiology of GH decline in the aging process is unclear, specifically, whether it results from decreased GHRH or increased SST levels. Similarly, it is not known whether quantitative changes in hypothalamic peptides (including SST) precede or follow age-related pathological behavioral changes. SST is produced mainly by cells of the central nervous system (CNS) and the gastrointestinal (GI) tract, which are functionally interconnected systems that undergo significant changes during aging. The physical changes in the aging organism are considered physiological, and experimental evidence indicates that a large proportion of these changes are the result of declining hormonal activity (including the SST system). It is particularly important to understand the role of SST in diseases of old age, which affect both cognitive processes and memory (e.g., Alzheimer's and Parkinson's diseases) and the proper functioning of the GI tract and pancreas (e.g., obesity, type 2 diabetes mellitus, and colorectal cancer). This narrative review discusses systemic and peripheral changes in SST production and secretion observed in aging individuals and their potential association with selected diseases of old age, especially CNS and GI tract diseases. Understanding the role of SST expression with age will enable the better application of this neuropeptide in the diagnosis and treatment of diseases of old age (including cancers). - Source: PubMed
Publication date: 2026/05/10
Kasprzak Aldona - Post-stroke edema is one of the fatal consequences of ischemic stroke where increased intracranial pressure can exacerbate neurological dysfunction leading to mortality. To date, conventional post-stroke therapy has failed to manage cerebral edema and render neuroprotection. Earlier, our lab reported the benefits of intra-arterially administered mesenchymal stem cells (IA MSCs) in alleviating post-stroke vasogenic edema. Recently, post-stroke neuroendocrine regulation involving growth hormone releasing hormone receptor (GHRH-R) analog is gaining attention as one of the potential targets for stroke intervention, adjunctive to the existing conventional therapies. Therefore, the current study aims to explore the combined therapeutic potential of IA MSCs and GHRH-R analogs in resolution of cerebral vasogenic edema following ischemic stroke. - Source: PubMed
Publication date: 2026/04/30
Datta AishikaGhosh BijoyaniKumari AnitaKarmarkar GautamMukherjee UshmitaDubey AkshadaBarik AnirbanSingh AnkitMalik NikitaSarmah DeepaneetaSchally Andrew VWangpaichitr MedhiSha WeiYavagal Dileep RBhattacharya Pallab