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Mouse (Murine) Polyclonal CRH Primary Antibody für 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 für 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 für 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 für 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
our results suggest an inhibitory role of miR (zeige MLXIP Antikörper)-212 on the HPA (zeige HPSE Antikörper) axis, which acts in a counter-regulatory manner.
Study shows that prolactin (zeige PRL Antikörper) 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 (zeige CRHR1 Antikörper). The antagonists caused a modest reduction of spontaneous excitatory transmission onto CA3 (zeige CA3 Antikörper) 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 (zeige PVALB Antikörper)(+) 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 (zeige GABRg1 Antikörper) receptor (GABAAR (zeige GABRG2 Antikörper)) and the Na(+)-K(+)-2Cl(-) cotransporter (zeige SLC12A1 Antikörper) (NKCC1 (zeige SLC12A2 Antikörper)), but not the K(+)-Cl(-) cotransporter (zeige SLC12A4 Antikörper) (KCC2 (zeige SLC12A5 Antikörper)), were expressed in the terminals of the CRH neurons at the median eminence (ME). In contrast, CRH neuronal somata were enriched with KCC2 (zeige SLC12A5 Antikörper) but not with NKCC1 (zeige SLC12A2 Antikörper).
Excitability of genetically isolated CRF-receptive (CRFR1 (zeige CRHR1 Antikörper)) neurons in the central nucleus of the amygdala (CeA (zeige CEA Antikörper)) is potently enhanced by CRF and that CRFR1 (zeige CRHR1 Antikörper) signaling in the CeA (zeige CEA Antikörper) is critical for discriminative fear
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 (zeige CRHR1 Antikörper) expression was significantly correlated with psychological stress in vitiligo (zeige MITF Antikörper).
Corticotrophin-releasing hormone accelerated tumor angiogenesis by upregulating VEGF (zeige VEGFA Antikörper) expression and secretion in colon cancer cells.
This study found that the expressions of CRH and CRHR1 (zeige CRHR1 Antikörper) 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 (zeige NGFB Antikörper); reduction of CRH and NGF (zeige NGFB Antikörper) may be under influence of sympathetic nervous system and may reflect deficit of neuronal stress-adaptation in PCOS patients. (NGF (zeige NGFB Antikörper) = 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 (zeige UCN Antikörper) and CRH-R2 (zeige CRHR2 Antikörper) mRNA levels were significantly higher than in ovarian endometrioma.
In summary, cardiac expression of CRFR1 (zeige CRHR1 Antikörper), CRF, and Ucn3 (zeige UCN3 Antikörper) genes is elevated in heart failure and may contribute to the activation of the CRF/Ucn (zeige UCN Antikörper) system in these patients.
VIP (zeige Vip Antikörper) and CRF reduce ADAMTS (zeige ADAMTS13 Antikörper) expression and function in osteoarthritis synovial fibroblasts.
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.
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 (zeige POMC Antikörper) 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
, C1q and tumor necrosis factor-related protein 14
, C1q related factor
, C1q-related factor
, C1q/TNF-related protein 14