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anti-Mouse (Murine) CRH Antibodies:
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Mouse (Murine) Polyclonal CRH Primary Antibody for IEM, ICC - ABIN617894
Preeyasombat, Sirikulchayanonta, Mahachokelertwattana, Sriphrapradang, Boonpucknavig: Cushing's syndrome caused by Ewing's sarcoma secreting corticotropin releasing factor-like peptide. in American journal of diseases of children (1960) 1992
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Human Monoclonal CRH Primary Antibody for ELISA, WB - ABIN514593
Wang, Parobchak, Rosen: RelB/NF-?B2 regulates corticotropin-releasing hormone in the human placenta. in Molecular endocrinology (Baltimore, Md.) 2012
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Human Polyclonal CRH Primary Antibody for ICC, IF - ABIN259726
El Yamani, Yon, Guérin, El Ouezzani, Alaoui, Chartrel, Anouar, Magoul et al.: Immunocytochemical distribution of EM66 within the hypothalamic parvocellular paraventricular nucleus: colocalization with CRH and TRH but no plasticity related to acute stress and thyroidectomy in ... in Regulatory peptides 2013
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Human Polyclonal CRH Primary Antibody for IF (p), IHC (p) - ABIN726800
Balan, Warnock, Puche, Gondre-Lewis, Aurelian: Innately activated TLR4 signal in the nucleus accumbens is sustained by CRF amplification loop and regulates impulsivity. in Brain, behavior, and immunity 2017
Hypothalamic CRH-expressing neurons orchestrate complex behaviors after stress.
Mice lacking corticotropin-releasing hormone, had an improved ability to escape away from potentially dangerous situations.
our results suggest an inhibitory role of miR-212 on the HPA axis, which acts in a counter-regulatory manner.
Study shows that prolactin was sufficient to suppress corticotrophin-releasing hormone (CRH) mRNA expression in the paraventricular nucleus, however it does not appear to be required for the ongoing regulation of the CRH neurones in lactation.
Study blocked endogenous CRH using 2 chemically distinct antagonists of the principal hippocampal CRH receptor, CRHR1. The antagonists caused a modest reduction of spontaneous excitatory transmission onto CA3 pyramidal cells, mediated. This was accompanied by a decrease in incidence but not amplitude of sharp waves, indicating that CRH synaptic actions are sufficient to alter the output of a complex hippocampal network.
Mice exposed to aggressive confrontations exhibited a similar pattern of species-typical aggressive and non-aggressive behaviors on the first and the last session. Repeated aggressive confrontations promoted an increase in plasma corticosterone. After 10 aggressive confrontation sessions, mice presented a non-significant trend toward reducing hippocampal levels of CRF, which inversely correlated with plasma corticosterone
Data (including data from studies in transgenic mice) suggest that Crh alters Gnrh neuron activity and that estradiol is required for Crh to exert both stimulatory and inhibitory effects on Gnrh neurons. (Crh = corticotropin-releasing hormone; Gnrh = gonadotropin releasing hormone)
The activation of parvalbumin(+) interneurons during morphine withdrawal was crucial for the induction of the negative emotion and the up-regulation of CRH mRNA levels in the central amygdala.
Psychological stress-derived CRF can breach the established endotoxin tolerance in the intestinal mucosa.
CRF plays a marked anxiogenic role at CRF1 receptors in the amygdala of mice exposed to the Elevated plus maze.
GABAA receptor (GABAAR) and the Na(+)-K(+)-2Cl(-) cotransporter (NKCC1), but not the K(+)-Cl(-) cotransporter (KCC2), were expressed in the terminals of the CRH neurons at the median eminence (ME). In contrast, CRH neuronal somata were enriched with KCC2 but not with NKCC1.
Excitability of genetically isolated CRF-receptive (CRFR1) neurons in the central nucleus of the amygdala (CeA) is potently enhanced by CRF and that CRFR1 signaling in the CeA is critical for discriminative fear
activation of the Gq-membrane-associated estrogen receptors rapidly stimulates hypothalamic paraventricular nucleus CRH neurons by suppressing the M-current and potentiating glutamatergic neurotransmission
Data describe a missing function of the stress hormone Crh in the regulation of autophagy activation and present evidence that this effect is linked to maintenance of gut homeostasis under basal conditions.
Real-time PCR analyses revealed that social defeat significantly increased corticotropin-releasing hormone in the paraventricular nucleus.
Data suggest a physiologically relevant role for local corticotropin-releasing hormone signaling towards shaping the neuronal circuitry within the mouse olfactory bulb.
results suggest that long-term, post-natal CRF over-expression increases the rewarding effects of cocaine in individuals with high emotional response to stress.
Knockdown of CRF synthesis in the ventral tegmental area prevented interpeduncular intermediate activation and anxiety during nicotine withdrawal.
selective disruption of Grin1 within central amygdala CRF neurons strongly enhances fear memory
it is shown that CRH and UCN upregulate galectin-1 expression in Ishikawa cell line and macrophages and this effect is mediated through CRHR1.
Early-preterm birth showed a syndrome of high maternal CRH and low vitamin D status.
REVIEW: CRF Family of Neuropeptides and their Receptors - Mediators of the Central Stress Response
REVIEW: Brain and Gut CRF Signaling: Biological Actions and Role in the Gastrointestinal Tract
REVIEW: The Multi-faceted Profile of Corticotropin-releasing Factor (CRF) Family of Neuropeptides and of their Receptors on the Paracrine/Local Regulation of the Inflammatory Response
Significant effects of CNS sensitization on CRF mRNA levels were detected in the Dorsal Striatum (increasing effect).
These results show epigenetic changes in the CRH gene related to severity of suicide attempt in adults and a general psychiatric risk score in adolescents.
Data suggest that corticotrophin-releasing hormone (CRH) is able to stimulate copeptin release in healthy controls suggesting direct interaction of CRH/CRH-receptor signaling and vasopressin; these interactions appear to be altered in patients with pituitary disease; copeptin may be serum biomarker of altered CRH/CRH-receptor signaling in pituitary diseases.
The development of disorders related to heightened stress sensitivity and dysregulation of stress-coping mechanisms appears to involve regulatory mechanisms of the CRH family members. The purpose of this review is to summarize the most significant discoveries related to CRH over time. [review]
A significant increase in CRH and CRHR-1 expression was significantly correlated with psychological stress in vitiligo.
Corticotrophin-releasing hormone accelerated tumor angiogenesis by upregulating VEGF expression and secretion in colon cancer cells.
This study found that the expressions of CRH and CRHR1 were significantly higher in the epileptogenic tissues of patients with IS than in the control group.
The authors propose that conditions impacting on epiallele distribution influence the number of transcriptionally active CRH gene copies in the trophoblast cell population determining the gestational trajectory of placental CRH production in normal and pathological pregnancies.
Neuroimmune-endocrine events may lead to overactivity of sympathetic nervous system that triggers cascade of pathologic conditions in ovary in polycystic ovary syndrome (PCOS). Data suggest that women with PCOS exhibit reduction of CRH and NGF; reduction of CRH and NGF may be under influence of sympathetic nervous system and may reflect deficit of neuronal stress-adaptation in PCOS patients. (NGF = nerve growth factor)
brain activation in response to colorectal distention is enhanced after CRH injection in Irritable bowel syndrome patients compared to healthy controls
In deep infiltrating endometriotic lesions, CRH, Ucn and CRH-R2 mRNA levels were significantly higher than in ovarian endometrioma.
In summary, cardiac expression of CRFR1, CRF, and Ucn3 genes is elevated in heart failure and may contribute to the activation of the CRF/Ucn system in these patients.
VIP and CRF reduce ADAMTS expression and function in osteoarthritis synovial fibroblasts.
This study localized a complete CRF system in the human fetal heart.
Placenta CRH mRNA concentration appears to convey information about the risk of brain damage in the infant born at an extremely low gestational age.
These results suggest that the CRH and CRH-BP genes have no direct effect on Irritable bowel syndrome status.
Evidence is provided for porcine corticotropin releasing hormone (CRH) as a quantitative trait locus (QTL) affecting growth and body composition. (corticotropin releasing hormone; CRH; CRF)
CRH inhibits local progesterone production from luteal cells in swine corpus lutem.
CRF-mediated cytoprotection occurs through the slow and tightly controlled apoptotic pathway.
We show that the CRF system is expressed in fish heart, is upregulated by hypoxia, and is cytoprotective.
Rigorous acute stressor stimuli induce behavioral changes, accompanied by an increase of cortisol levels with delayed control of CRH mRNA expression.
CRF localized in the preoptic area, periventricular hypothalamic and tectal regions, and dorsal part of the trigeminal motor nucleus.
The results of this study indicated that chronic CRF overexpression in primates not only increases Anxious Temperament but also affects metabolism and connectivity within components of Anxious Temperament 's neural circuitry.
We show that -2232C>G alters DNA x protein interactions and confers decreased sensitivity of the CRH promoter to glucocorticoids in vitro.
Data suggest that CRH promoter variation that confers increased stress reactivity increases the risk for alcohol use disorders in stress-exposed individuals.
The association has been reported between polymorphisms of the CRH and POMC genes with economic traits in Korean cattle.
CRH is a promising candidate gene for a concordant QTL related to lipid metabolism in mammals.
corticotropin-releasing factor mRNA fluctuated with food intake in the hypothalamus, pretectum, and optic tectum; CRF mRNA decreased 6 h after a meal and remained low through 31 days of food deprivation
Corticotropin-releasing hormone is secreted by the paraventricular nucleus (PVN) of the hypothalamus in response to stress. Marked reduction in this protein has been observed in association with Alzheimer disease and autosomal recessive hypothalamic corticotropin deficiency has multiple and potentially fatal metabolic consequences including hypoglycemia and hepatitis. In addition to production in the hypothalamus, this protein is also synthesized in peripheral tissues, such as T lymphocytes and is highly expressed in the placenta. In the placenta it is a marker that determines the length of gestation and the timing of parturition and delivery. A rapid increase in circulating levels of the hormone occurs at the onset of parturition, suggesting that, in addition to its metabolic functions, this protein may act as a trigger for parturition.
, corticotropin releasing factor
, corticotropin-releasing factor
, corticotropin-releasing hormone
, corticotropin releasing hormone
, corticotrophin-releasing factor
, corticotropin releasing hormone, gene 1
, corticotropin-releasing factor b
, corticotropin releasing hormone b
, Corticotropin-releasing hormone
, corticotropin releasing hormone a
, corticotropin-releasing factor a