ACTH (1-14) -

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207.62 €

Known as:: ACTH (1-14) -
Catalog number:: 06-271-83033
Product Quantity:: 1 mg
Category:: -
Supplier:: GenWay
Gene target:: ACTH (1-14) -

Related genes to: ACTH (1-14) -

Gene:: ADGRG5 ^{NIH gene}
Name:: adhesion G protein-coupled receptor G5
Previous symbol:: GPR114
Synonyms:: PGR27
Chromosome:: 16q21
Locus Type:: gene with protein product
Date approved:: 2002-11-26
Date modifiied:: 2016-10-05

Gene:: ARHGEF18 ^{NIH gene}
Name:: Rho/Rac guanine nucleotide exchange factor 18
Previous symbol:: -
Synonyms:: P114-RhoGEF, KIAA0521, MGC15913
Chromosome:: 19p13.2
Locus Type:: gene with protein product
Date approved:: 2004-01-09
Date modifiied:: 2016-10-04

Gene:: ARMH3 ^{NIH gene}
Name:: armadillo like helical domain containing 3
Previous symbol:: C10orf76
Synonyms:: FLJ13114
Chromosome:: 10q24.32
Locus Type:: gene with protein product
Date approved:: 2004-02-17
Date modifiied:: 2019-02-21

Gene:: ASS1P11 ^{NIH gene}
Name:: argininosuccinate synthetase 1 pseudogene 11
Previous symbol:: ASSP11
Synonyms:: TCAG_1641141
Chromosome:: 7p15.3
Locus Type:: pseudogene
Date approved:: 1986-01-01
Date modifiied:: 2014-11-19

Gene:: BPIFB1 ^{NIH gene}
Name:: BPI fold containing family B member 1
Previous symbol:: C20orf114
Synonyms:: dJ1187J4.1, MGC14597, bA49G10.6, LPLUNC1, VEMSGP
Chromosome:: 20q11.21
Locus Type:: gene with protein product
Date approved:: 2001-07-17
Date modifiied:: 2015-12-07

Related products to: ACTH (1-14) -

Related articles to: ACTH (1-14) -

Perinatal Organophosphate Flame Retardant Exposure Alters Adult Stress Axis and Avoidance Behavior in Mice.
Organophosphate flame retardants (OPFRs) are ubiquitous flame-retardant additives with endocrine-disrupting properties. Despite increasing evidence that OPFRs impact neurodevelopment, their effects on the neuroendocrine stress response remain poorly understood. To examine their long-term impact on stress regulation, we treated pregnant C57Bl/6J dams to a mixture of tris(1,3-dichloro-2-propyl) phosphate (TDCPP), triphenyl phosphate (TPP), and tricresyl phosphate (TCP; 1 mg/kg each) from gestational day (GD) 7 through postnatal day (PND) 14. Adult offspring (8-9 weeks of age) were then challenged with acute stressors, including 1 h restraint or a 6-day acute variable stress (AVS) paradigm. Perinatal OPFR exposure produced persistent, sex-specific alterations in the hypothalamic-pituitary-adrenal (HPA) axis and stress-related neurocircuitry. Following 1 h restraint, OPFR-treated females showed heightened serum corticosterone. In addition, gene expression analysis revealed sex-dependent disruptions in key stress-regulatory pathways after OPFR treatment and 1 h restraint in the hypothalamus (Crhr1, Crhr2, Ptpn5) and pituitary (Crhr1, Pomc, Nr3c1). Females demonstrated more differences in adrenal gene expression related to steroidogenesis (Mc2r, Cyp11b2) and catecholamine biosynthesis (Dbh, Pnmt), with OPFR-treated groups having blunted responses. OPFR AVS females displayed reduced corticosterone and Crh mRNA in the hypothalamus, and downregulated Pacap/Pac1r expression in the bed nucleus of the stria terminalis (BNST), accompanied by increased behavioral avoidance and immobility. In males, OPFR exposure led to increased BNST Pacap and Pac1r, expression, along with hyperactivity and avoidance behaviors. Together, these findings demonstrate that early-life OPFR exposure induces lasting, sex-specific dysregulation of the HPA axis and associated stress circuits, highlighting OPFRs as developmental neuroendocrine disruptors with implications for mood and stress-related disorders. - Source: PubMed
Publication date: 2026/05/06
Rojas Catherine MDeLucca JuliaBrown Caylee AYasrebi AliChiou SavannahBello Nicholas TRoepke Troy A
Retinal ganglion cell degeneration in glaucoma disrupts HPA axis temporal organization and dampens corticosterone production.
Glaucoma is a chronic optic neuropathy characterized by progressive vision loss. A previous study from our group showed that glaucoma-induced retinal degeneration disrupts photic signaling to the suprachiasmatic nucleus (SCN), altering the molecular components of the central circadian clock. Through its hypothalamic projections, the SCN entrains the hypothalamic-pituitary-adrenal (HPA) axis and drives the rhythmic secretion of corticosterone. In this study, we investigated whether central circadian clock disruption in glaucoma impacts the HPA axis and its downstream physiological rhythms. We analyzed the temporal profiles of key genes controlling the HPA axis in mice with glaucoma. The Crh gene expression was reduced in the paraventricular nucleus, while Crh-r1 exhibited a 10-h phase delay in the pituitary in response to glaucoma. Additionally, Pomc in the pituitary and Mc2r in the adrenal lost rhythmicity. The modulation of the daily rhythms of these key genes was associated with alterations in the diurnal rhythms of clock genes in the PVN, pituitary and adrenal gland. Glaucoma-induced phase shifts and amplitude alterations in the rhythmic expression of Per1, Per2, Nr1d1, and Bmal1 in the pituitary and adrenal gland, resulted in a temporal misalignment between the pituitary and adrenal rhythms. These molecular changes were associated with reduced corticosterone amplitude, suggesting impaired communication between central and peripheral clocks. Together, these findings demonstrate that glaucoma alters the temporal coordination of the HPA axis, highlighting how retinal dysfunction can propagate beyond the visual system to disturb systemic circadian and neuroendocrine regulation. - Source: PubMed
Barsanele Pietra Souzada Silva Juliano JeffersonCortes Bryan Fellipe da Silvade Oliveira Furtado Eliz MariaCipolla-Neto Joséde Assis Leonardo Vinícius MonteiroPoletini Maristela OliveiraMoraes Maria Nathália
Diet-associated modulation of HPI axis gene expression and POMC paralogs in gilthead seabream.
The hypothalamic-pituitary-interrenal (HPI) axis mediates stress responses in fish. Previous work showed that dietary supplementation with B vitamins attenuated cortisol response to acute stress, whereas dietary genistein produced high basal levels of cortisol and altered stress responsiveness. In the present study, we investigated the expression of key genes of the HPI axis and selected hepatic targets to better characterize these responses. Cortisol was correlated with nr3c1 expression in the pituitary of control fish. Conversely, B vitamins supplementation was associated with changes in the relationship between plasma cortisol levels and nr3c1 expression across tissues, including higher basal higher basal expression expression in the head kidney. In parallel, lower hepatic oxidative stress following acute stress in this fish was associated with differences in cortisol levels and liver metabolic responses. Dietary genistein was associated with altered pituitary regulation of pomc paralogs, characterized by reduced pomcb and elevated pomca expression after stress. These expression patterns persisted 4.5 months after dietary exposure, with pomca becoming the only gene showing a positive association with plasma cortisol levels. In addition, genistein supplementation was associated with higher basal expression of the ACTH receptor (mc2r) in the head kidney. Stress challenges performed up to one year after the nutritional intervention revealed convergence of cortisol responses among dietary groups. Overall, these results indicate that dietary components can produce short-term changes in the regulation of the HPI axis. Further studies are required to clarify the mechanisms underlying the dietary effects observed in this study. - Source: PubMed
Publication date: 2026/02/19
Navarro-Guillén CarmenHuesa-Cerdán RubénHidalgo-Pérez Juan AntonioMartínez-Rodríguez GonzaloRodríguez-Viera LeandroMartos-Sitcha Juan AntonioBlanco-Benítez Juan JoséPerera Erick
Neonatal lipopolysaccharide administration causes long-term changes in mouse immunosteroids.
Early-life infections have enduring effects on the immune and endocrine systems. Glucocorticoids (GCs) are produced by the adrenal glands and also produced by lymphoid organs (immunosteroids). We investigated the impacts of early-life lipopolysaccharide (LPS) challenge on GC and mineralocorticoid regulation in blood and lymphoid organs. We administered saline vehicle (nVEH) or LPS (50 µg/kg body wt, ip) (nLPS) to neonatal mice on postnatal day (PND) 4 and 6 ("first hit"). We then administered saline vehicle (aVEH) or LPS (50 µg/kg body wt, ip) (aLPS) to adults on PND90 ("second hit"), in a 2 × 2 design. We collected whole blood, bone marrow, thymus, and spleen 4 h after treatment at PND90. We measured nine steroids via liquid chromatography-tandem mass spectrometry and measured transcripts of steroidogenic enzymes (, , , and ), GC receptor, mineralocorticoid receptor, and hypothalamic-pituitary-adrenal axis components (, , , and ) via RT-qPCR. The nLPS treatment did not have significant effects on blood GC levels in adulthood. Nonetheless, nLPS treatment increased corticosterone and 11-dehydrocorticosterone levels in lymphoid organs of aLPS subjects. The nLPS treatment increased aldosterone levels in blood and bone marrow of aVEH females but decreased aldosterone levels in bone marrow and thymus of aVEH males. The nLPS treatment also increased transcripts for steroidogenic enzymes, especially the aldosterone-synthetic enzyme , and modulated transcripts for steroid receptors, especially mineralocorticoid receptors, in lymphoid organs of aVEH and aLPS subjects. These findings suggest that elevated local GC and aldosterone production in lymphoid organs is a mechanism for the enduring effects of early-life infections on immune function. Using a "two-hit" model in mice, we examined the effects of early-life lipopolysaccharide (LPS) administration on steroid regulation in blood and lymphoid organs. Mice received saline or LPS as neonates, and then saline or LPS as adults. Neonatal LPS heightened local glucocorticoid and systemic aldosterone responses to adult LPS treatment in bone marrow, thymus, and spleen. These data highlight the potential role of immunosteroids in developmental programming of immune function and health. - Source: PubMed
Publication date: 2026/01/07
Salehzadeh MelodyMazurenko AnnaSoma Kiran K
Mild Neonatal Hypoxia Modifies the Reactivity of the Glucocorticoid System in Adult Rats, Promoting Improved Learning and Spatial Memory Under Stressful Conditions.
Mild neonatal hypoxia (NH) can serve as a conditioning stimulus that persistently modulates stress systems. We tested whether brief neonatal hypobaric hypoxia induces long-term changes hypothalamic-pituitary-adrenal (HPA) regulation and adult behavior. Male Wistar rats received three 2 h hypobaric sessions on postnatal days 8-10. At 3 months, behavior was assessed. Biochemical measures included plasma/adrenal corticosterone (CORT), plasma ACTH, brain CORT, CRH/POMC/GR/11β-HSD2 protein, and HPA/steroidogenic gene expression. NH yielded a calmer, context-beneficial phenotype: startle latency increased, Morris water maze memory improved, whereas Barnes, recognition memory, and forced swim measures were unchanged. Hypothalamic CRH protein and pituitary/plasma ACTH were reduced, despite unchanged crh and Pomc mRNA, suggesting post-transcriptional control. Basal CORT in plasma and adrenals remained unchanged, but the CORT response to mild stress was larger and more sustained. In the adrenal glands, Cyp11b1 was selectively downregulated, whereas Mc2r, Cyp11a1, Hsd3b2, Cyp21a1 were unaffected. GR and 11β-HSD2 protein did not differ across tissues. In the brain, CORT decreased selectively in the amygdala. NH appears to act as developmental preconditioning, leading to persistent behavioral adaptations and altered HPA regulation in adulthood, characterized by reduced central drive at rest, preserved basal output, and efficient mobilization under challenge. - Source: PubMed
Publication date: 2026/01/07
Potapova SofiyaSafarova DianaTyulkova EkaterinaVetrovoy Oleg

ACTH (1-14) -

Related genes to: ACTH (1-14) -

Related products to: ACTH (1-14) -

Related articles to: ACTH (1-14) -

Perinatal Organophosphate Flame Retardant Exposure Alters Adult Stress Axis and Avoidance Behavior in Mice.

Retinal ganglion cell degeneration in glaucoma disrupts HPA axis temporal organization and dampens corticosterone production.

Diet-associated modulation of HPI axis gene expression and POMC paralogs in gilthead seabream.

Neonatal lipopolysaccharide administration causes long-term changes in mouse immunosteroids.

Mild Neonatal Hypoxia Modifies the Reactivity of the Glucocorticoid System in Adult Rats, Promoting Improved Learning and Spatial Memory Under Stressful Conditions.