Polyclonal Rabbit CRHR2 Antibody
- Known as:
- Polyclonal Rabbit CRHR2 Antibody
- Catalog number:
- KA0904
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit CRHR2 Antibody
Related genes to: Polyclonal Rabbit CRHR2 Antibody
- Gene:
- CRHR2 NIH gene
- Name:
- corticotropin releasing hormone receptor 2
- Previous symbol:
- -
- Synonyms:
- CRF2, CRF-RB, HM-CRF
- Chromosome:
- 7p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-18
- Date modifiied:
- 2015-08-26
Related products to: Polyclonal Rabbit CRHR2 Antibody
Related articles to: Polyclonal Rabbit CRHR2 Antibody
- Acquired chronic disease is a significant, growing problem. Research has sought patient abnormalities that drugs can target, but to date, these have only provided equivocal symptom relief and no cures. However, as individual neuronal signals cannot be measured, the role of the brain in such diseases, has not been properly investigated. Here the authors propose that corticotropin-releasing factor (CRF) and serotonin act together in dedicated circuits, to architect precise, signals that regulate normal function (e.g., thermoregulation, movement, memory, glomerular filtration rate). The authors propose further that the natural, circuit-specific upregulation of the CRF receptor type 2 (CRFR2), dysregulates these signals to cause chronic symptoms (e.g., low temperature, impaired movement, memory loss, reduced glomerular filtration rate). If confirmed, this view of chronic symptoms as a dysregulation of normal process via neuronal adaptation, has profound implications. It could explain Parkinson's, Alzheimer's and chronic kidney disease, among others, and, as it may be possible to downregulate CRFR2, could reverse the signs and symptoms of such diseases. - Source: PubMed
Publication date: 2026/04/13
Pereira GerardCorbett MichaelVernon Suzanne DColburn ShaunChanda Sanjay - Neuropathic pain is a debilitating condition that lacks effective treatments. Corticotropin-releasing hormone (CRH) is associated with the central neural circuits involved in stress and pain. Here, we identified a peripheral CRH-mediated signaling axis in dorsal root ganglion (DRG) and spinal neurons underlying neuropathic pain. Spared nerve injury (SNI) in male mice increased the abundance of CRH in small- and medium-diameter DRG neurons, specifically in their central terminals in the spinal dorsal horn. DRG-specific knockdown of CRH alleviated neuropathic pain. SNI increased expression by inducing the binding of the transcription factor SMAD1 to the promoter. Silencing SMAD1 in the DRG reduced neuropathic pain symptoms, which was accompanied by a decrease in the amount of CRH in the DRG tissue. Pharmacological antagonism of CRH receptor 2 (CRHR2), but not of CRHR1, attenuated neuropathic pain and suppressed the activation of spinal neurons and glia. Spinal CRHR2 predominantly localized to excitatory neurons and somatostatin-positive interneurons in the superficial dorsal horn. These findings reveal a SMAD1-CRH-CRHR2 axis in DRG-to-spine signaling that promotes neuropathic pain and suggest that CRHR2 antagonists be explored for its management. - Source: PubMed
Publication date: 2026/04/28
He ChengMa Ling-JieFu Yuan-YuanZhang Ke-ChenTao YeWei XiaoShen Yong-LiangWang JuanGao Yong-JingZhang Zhi-Jun - Females are 2-3 times more likely than males to be diagnosed with mood disorders, including depression and anxiety, yet the neurobiological mechanisms contributing to this sex difference are not fully understood. Corticotropin-releasing factor receptor 2 (CRFR2) plays a key role in regulating stress responses, with evidence suggesting it may dampen hypothalamic-pituitary-adrenal (HPA) axis activation and behavioral stress responses. Although CRFR2 has been implicated in stress buffering, little is known about how its expression and activation differs by sex, particularly in the mouse model. To address this gap, we used newly generated CRFR2-Cre-2α-TdTomato mice to investigate sex differences in CRFR2-expressing neurons and their activation across stress-regulating brain regions following an acute restraint. Males exhibited significantly more CRFR2-expressing neurons in the lateral septum, bed nucleus of the stria terminalis, paraventricular nucleus of the hypothalamus, and central amygdala, while females had more CRFR2-expressing neurons in the medial amygdala and ventromedial hypothalamus. Activation of CRFR2 neurons also showed region-specific sex differences, with males generally exhibiting greater CRFR2 colocalization with c-Fos, a marker for neural activation. Corticosterone levels following restraint were correlated with CRFR2 expression or activation in several brain regions, including the paraventricular hypothalamus, medial amygdala, and bed nucleus of the stria terminalis. These findings identify novel sex differences in CRFR2 expression and stress-induced activation of CRFR2 neurons across multiple stress-regulating brain areas. Together, these results suggest that sex differences in CRFR2 signaling may mediate sex differences in HPA axis responsivity as well as behavioral stress responses. - Source: PubMed
Publication date: 2026/02/28
Lafrican Jennifer JParra Katherine ERybka Krystyna ALadison Jayden MHellman Noah AAmato EnricoTaroc Ed Zandro MKolaib Alzahra SThayer RhiannonSakeria Angela AMeunier PaulineZuloaga Kristen LForni Paolo EJustice Nicholas JZuloaga Damian G - Corticotropin-releasing hormone (CRH) and its receptors CRHR1 and CRHR2 are major actors in the stress response and are well established as components of the hypothalamic-pituitary-adrenal (HPA) axis. Evidence also suggests they are expressed in peripheral tissues and, more interestingly, in the skin. While CRHR1 expression in keratinocytes is documented in terms of presence or absence, data on CRHR2 remain sparse. Moreover, there is no detailed description of the exact localization of CRHR1/2 receptors within the different layers of the epidermis, leaving this question fully unexplored. To better understand the link between stress and skin disorders, we aimed to investigate the differential expression of CRHR1 and CRHR2 in keratinocytes, depending on their level of differentiation. In vitro results demonstrated that CRHR1 appears to be more abundant at early stages of differentiation and CRHR2 at more advanced stages. - Source: PubMed
Publication date: 2026/02/14
Martins Carole-AnneLesink SaraRoux AngélineCollet GuillaumeDaniellou Richard - Early life pain and stress have lasting consequences on nervous system development that can interact with later stress or trauma to create a susceptibility to fear, anxiety, depression and chronic pain among other psychological disorders. Recent work has identified changes in corticotropin releasing factor signaling in limbic system structures, such as the amygdala and hypothalamus, as a key mechanism behind these changes - albeit in a sex-dependent manner. CRF has two major receptors, CRFR1 and CRFR2 which have also been shown to play key roles in fear and pain expression. The current work examines the effects of early life pain designed to mimic the neonatal medical trauma that occurs in the Neonatal Intensive Care Unit (NICU), paired with a juvenile trauma in the form of fear conditioning, on expression of crhr1 and crhr2 mRNA in the central nucleus (CeA) and basolateral nucleus (BLA) of the amygdala as well as the paraventricular nucleus (PVN) and ventromedial nucleus (VMH) hypothalamus of the juvenile rat. While prior work has demonstrated that early life pain significantly impacts expression of the CRF ligand mRNA, this study examines the effects of early life pain and stress, as well as adolescent fear conditioning, on CRF receptor expression. The data demonstrate that early life pain and fear conditioning have only modest effects on CRF receptor expression in the amygdala and hypothalamus in a sex dependent manner. In both sexes, fear conditioning increased crhr2 mRNA in the CeA only in neonatally undisturbed subjects. In addition, there was a trend towards altered crhr2 mRNA following neonatal manipulation in the PVN. In females specifically, we observed significant changes in crhr2 mRNA expression following fear conditioning in the right BLA. There were no female-specific changes following neonatal pain and stress. In males, we observed significant changes in crhr1 mRNA in the posterior PVN and trends toward changes in crhr2 mRNA in the CeA and VMH following neonatal manipulation. Together, these data confirm prior work that early life pain and stress alter the neural circuitry of pain and stress in a sex-specific manner. However, given the limited changes observed, in it unlikely that CRH receptor alterations are a major mechanism of action of early life pain. - Source: PubMed
Publication date: 2026/02/23
Burman Michael AZuke Jared T