Results 41 to 50 of about 4,400 (198)

Dependence of fertility on kisspeptin–Gpr54 signaling at the GnRH neuron [PDF]

open access: yesNature Communications, 2013
Signaling between kisspeptin and its receptor, G-protein-coupled receptor 54 (Gpr54), is now recognized as being essential for normal fertility. However, the key cellular location of kisspeptin-Gpr54 signaling is unknown. Here we create a mouse with a GnRH neuron-specific deletion of Gpr54 to assess the role of gonadotropin-releasing hormone (GnRH ...
Milen, Kirilov   +7 more
openaire   +2 more sources

The testosterone-dependent and independent transcriptional networks in the hypothalamus of Gpr54 and Kiss1 knockout male mice are not fully equivalent

open access: yesBMC Genomics, 2011
Background Humans and mice with loss of function mutations in GPR54 (KISS1R) or kisspeptin do not progress through puberty, caused by a failure to release GnRH.
Sutcliffe Margaret   +13 more
doaj   +1 more source

ارزیابی جهش های ژن GPR54 در دختران ایرانی با بلوغ زودرس فامیلیال [PDF]

open access: yesMajallah-i Zanān, Māmā̓ī va Nāzā̓ī-i Īrān, 2012
مقدمه: مسیر انتقال پیام GPR54/Kisspeptin به عنوان دروازه و تنظیم کننده فعالیت نورون های آزاد کننده گونادوتروپین و عامل کلیدی شروع بلوغ می باشد. جهش های از دست دهنده عملکرد در ژن گیرنده متصل شونده به پروتیین GPR54 )G با تأخیر بلوغ مرکزی و جهش های کسب ...
نصرت قائمی   +4 more
doaj   +1 more source

Expression patterns of kiss2 and gpr54‐2 in Monopterus albus suggest these genes may play a role in sex reversal in fish

open access: yesFEBS Open Bio, 2019
Due to its exceptionally small genome size and protogynous hermaphroditism, Monopterus albus has been proposed as a model for vertebrate sexual development.
Ti‐Lin Yi   +2 more
doaj   +1 more source

Hypothalamic KiSS1/GPR54 Gene Expressions and Luteinizing Hormone Plasma Secretion in Morphine Treated Male Rats [PDF]

open access: yesInternational Journal of Fertility and Sterility, 2018
Background: The inhibitory effects of morphine and the stimulatory influence of kisspeptin signaling have been demonstrated on gonadotropin releasing hormone (GnRH)/luteinizing hormone (LH) release.
Homayoun Khazali   +2 more
doaj   +1 more source

Functional characterization of endogenous GPR54 mutants

open access: yesThe FASEB Journal, 2007
Increasing evidence suggests that the G‐protein coupled receptor GPR54, along with its ligand kisspeptin, play a pivotal role in the signaling cascade that initiates puberty. Accordingly, a small percentage of cases of isolated hypogonadotrophic hypogonadism (IHH) are caused by homozygous recessive mutations in human GPR54.
Jennifer L Wacker   +2 more
openaire   +1 more source

Chapter 2 Human Diseases Associated with GPR54 Mutations

open access: yes, 2009
G protein‐coupled receptor 54 (GPR54) was first described as an orphan receptor in the rat brain one decade ago. At that time, all we knew about this receptor was that it had a high homology with other G protein‐coupled receptors, like galanin receptors.
Suzy Bianco   +10 more
core   +1 more source

KNDy kisspeptin is required for metabolic homeostasis in female mice in an ovarian hormone‐independent manner

open access: yesJournal of Neuroendocrinology, Volume 38, Issue 6, June 2026.
Abstract Disorders of gonadotropin pulsatility contribute to reproductive dysfunction in humans and are often associated with metabolic dysfunction. Hypogonadotropic hypogonadism is characterized by chronically insufficient gonadotropin hormone production, leading to reproductive and metabolic impairments, such as infertility and obesity.
Nimisha Nandankar   +7 more
wiley   +1 more source

The genes associated with gonadotropin-releasing hormone-dependent precocious puberty [PDF]

open access: yesKorean Journal of Pediatrics, 2012
Human puberty is a complex, coordinated biological process with multiple levels of regulations. The timing of puberty varies greatly in children and is influenced by both environmental and genetic factors.
Jin Soon Hwang
doaj   +1 more source

Hyperoside Modulates the Estrogen‐PI3K/VEGF Axis to Ameliorate Oxidative Damage‐Induced Inhibition of Bone Formation in MC3T3‐E1 Cells

open access: yesImmunity, Inflammation and Disease, Volume 14, Issue 4, April 2026.
This study explores the potential of hyperoside to activate the estrogen‐PI3K/VEGF axis, thereby suppressing oxidative stress and enhancing osteogenic differentiation to mitigate osteoporosis. The initial proposal of the estrogen‐PI3K/VEGF signaling pathway axis as a potential therapeutic approach for osteoporosis.
Shuo Wang   +8 more
wiley   +1 more source

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