CLIA kit Corticotropin-releasing factor-binding protein,Corticotropin-releasing hormone-binding protein,CRF-binding protein,CRF-BP,Crhbp,CRH-BP,Mouse,Mus musculus
- Known as:
- CLIA reagent Corticotropin-releasing factor-binding protein,Corticotropin-releasing hormone-binding protein,CRF-binding protein,CRF-BP,Crhbp,CRH-BP,Mouse,Mus musculus
- Catalog number:
- U2166m
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- EIAab
- Gene target:
- CLIA kit Corticotropin-releasing factor-binding protein hormone-binding CRF-binding CRF- Crhbp CRH- Mouse Mus musculus
Related genes to: CLIA kit Corticotropin-releasing factor-binding protein,Corticotropin-releasing hormone-binding protein,CRF-binding protein,CRF-BP,Crhbp,CRH-BP,Mouse,Mus musculus
- Gene:
- BAZ1A NIH gene
- Name:
- bromodomain adjacent to zinc finger domain 1A
- Previous symbol:
- -
- Synonyms:
- hACF1, ACF1, WALp1, WCRF180
- Chromosome:
- 14q13.1-q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-06
- Date modifiied:
- 2018-02-13
- Gene:
- C1QL1 NIH gene
- Name:
- complement C1q like 1
- Previous symbol:
- -
- Synonyms:
- CRF, C1QRF, C1QTNF14, CTRP14
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-06
- Date modifiied:
- 2018-07-16
- Gene:
- CARHSP1 NIH gene
- Name:
- calcium regulated heat stable protein 1
- Previous symbol:
- -
- Synonyms:
- CRHSP-24, CSDC1
- Chromosome:
- 16p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-06-11
- Date modifiied:
- 2015-11-09
- Gene:
- CRH NIH gene
- Name:
- corticotropin releasing hormone
- Previous symbol:
- -
- Synonyms:
- CRF, CRH1
- Chromosome:
- 8q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-31
- Date modifiied:
- 2016-10-25
- Gene:
- CRHBP NIH gene
- Name:
- corticotropin releasing hormone binding protein
- Previous symbol:
- -
- Synonyms:
- CRF-BP, CRFBP
- Chromosome:
- 5q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-07
- Date modifiied:
- 2014-12-19
Related products to: CLIA kit Corticotropin-releasing factor-binding protein,Corticotropin-releasing hormone-binding protein,CRF-binding protein,CRF-BP,Crhbp,CRH-BP,Mouse,Mus musculus
Related articles to: CLIA kit Corticotropin-releasing factor-binding protein,Corticotropin-releasing hormone-binding protein,CRF-binding protein,CRF-BP,Crhbp,CRH-BP,Mouse,Mus musculus
- In the pejerrey Odontesthes bonariensis (Atheriniformes, Atherinopsidae), exposure to high and low temperatures during the critical period of sex determination (CPSD) induce testicular and ovarian differentiation, respectively, regardless of the presence or not of the sex determining gene amhy, which is crucial for testis formation only at intermediate, sexually neutral temperatures. In this study we explored the existence of genotype-specific signaling of Crh (Corticotropin Releasing Hormone) family genes and their associated carrier protein, receptors, and other stress-related genes in response to temperature during the CPSD and the potential involvement of the central nervous system via the hypothalamus-pituitary-interrenal (HPI) axis in the sex determination of this species. The Crh family genes crhb, uts1, ucn3, the receptor crhr1 and the stress-related genes gr1, gr2, nr3c2 were transiently upregulated in the heads of pejerrey larvae during the CPSD by high temperature alone or in combination with other factors. Only crhr2 transcript abundance was not influenced by temperature but independently by time and genotype. In most cases, mRNA abundance was higher in the XX heads compared to that of XY individuals. The mRNAs of some of these genes were localized in the hypothalamus of pejerrey larvae during the CPSD. XX larvae also showed higher whole-body cortisol titers than the XY, downregulation of cyp19a1a and upregulation of the testis-related genes amhy/amha in trunks (gonads) and were 100% masculinized at the high temperature. In contrast, at the low temperature, crhbp and avt were upregulated in the heads, particularly the former in XY larvae. cyp19a1a and amhy/amha were up- and downregulated, respectively, in the gonads, and fish were 100% feminized. Signaling via the HPI axis was observed simultaneously with the first molecular signs of ongoing sex determination/differentiation in the gonads. Overall, the results strongly suggest a temperature-dependent, genotype-specific regulatory action of the brain involving the Crh family of stress-related genes on the process of environmental sex determination of pejerrey. - Source: PubMed
Publication date: 2023/11/24
Torres-Martínez AarónHattori Ricardo ShoheiFernandino Juan IgnacioSomoza Gustavo ManuelHung Song DongMasuda YukiYamamoto YojiStrüssmann Carlos Augusto - Inflammation stimulates the hypothalamic-pituitary adrenal (HPA) axis and triggers glial neuroinflammatory phenotypes, which reduces monoamine neurotransmitters by activating indoleamine 2,3-dioxygenase enzyme. These changes can induce psychiatric diseases, including anxiety. Corticotropin releasing hormone receptor 2 (CRHR2) in the HPA axis is involved in the etiology of anxiety. Omega(n)-3 polyunsaturated fatty acids (PUFAs) can attenuate anxiety through anti-inflammation and HPA axis modulation. However, the underlying molecular mechanism by CRHR2 modulates anxiety and its correlation with neuroinflammation remain unclear. Here, we first constructed a crhr2 zebrafish mutant line, and evaluated anxiety-like behaviors, gene expression associated with the HPA axis, neuroinflammatory response, neurotransmitters, and PUFAs profile in crhr2 and crhr2 zebrafish. The crhr2 deficiency decreased cortisol levels and up-regulated crhr1 and down-regulated crhb, crhbp, ucn3l and proopiomelanocortin a (pomc a) in zebrafish. Interestingly, a significant increase in the neuroinflammatory markers, translocator protein (TSPO) and the activation of microglia M1 phenotype (CD11b) were found in crhr2 zebrafish. As a consequence, the expression of granulocyte-macrophage colony-stimulating factor, pro-inflammatory cytokines vascular endothelial growth factor, and astrocyte A1 phenotype c3 were up-regulated. While microglia anti-inflammatory phenotype (CD206), central anti-inflammatory cytokine interleukin-4, arginase-1, and transforming growth factor-β were downregulated. In parallel, crhr2-deficient zebrafish showed an upregulation of vdac1 protein, a TSPO ligand, and its downstream caspase-3. Furthermore, 5-HT/5-HIAA ratio was decreased and n-3 PUFAs deficiency was identified in crhr2 zebrafish. In conclusion, anxiety-like behavior displayed by crhr2-deficient zebrafish may be caused by the HPA axis dysfunction and enhanced neuroinflammation, which resulted in n-3 PUFAs and monoamine neurotransmitter reductions. - Source: PubMed
Publication date: 2023/08/26
Deng ShuyiGuo AnqiHuang ZhengweiGuan KaiyuZhu YaChan CheekaiGui JianfangSong CaiLi Xi - Suicide behavior (SB) emerge from complex interactions among traumatic events and multiple genetic factors. We conducted the first systematic review to assess the evidence of a link among trauma exposure, HPA-axis genes, and SB. A systematic search of PubMed, EBSCO, Science Direct, PsychInfo, and Scopus databases on gene-environment interaction, and susceptibility to SB was carried out until February 2022. Our study was prospectively registered in PROSPERO (CRD42022316141). A total of 13 epidemiological studies (11,756 subjects) were included: eight studies focused on traumatic experiences in the childhood and five studies on lifetime trauma exposure. All studies reported a positive association between the trauma exposure with SB. Gene-environment interaction was reported for CRHR1 (n = 6), CRHR2 (n = 2), FKBP5 (n = 2), and CRHBP (n = 1), however, for CRH, NR3C1, MC2R, and POMC genes no found gene-environment effects on SB. Trauma exposure could be one mechanism that links HPA-axis genes activity with the development of SB. - Source: PubMed
Publication date: 2023/06/15
González-Castro Thelma BeatrizJuárez-Rojop Isela EstherTovilla-Zárate Carlos AlfonsoOvando-Ricárdez José AntonioHernández-Díaz YazminLópez-Narváez María LiliaGenis-Mendoza Alma DeliaRodríguez-Pérez Candelario - Chronic post-traumatic musculoskeletal pain (CPTP) is a common outcome of traumatic stress exposure. Biological factors that influence the development of CPTP are poorly understood, though current evidence indicates that the hypothalamic-pituitary-adrenal (HPA) axis plays a critical role in its development. Little is known about molecular mechanisms underlying this association, including epigenetic mechanisms. Here, we assessed whether peritraumatic DNA methylation levels at 248 5'-C-phosphate-G-3' (CpG) sites in HPA axis genes (FKBP5, NR3C1, CRH, CRHR1, CRHR2, CRHBP, POMC) predict CPTP and whether identified CPTP-associated methylation levels influence expression of those genes. Using participant samples and data collected from trauma survivors enrolled into longitudinal cohort studies (n = 290), we used linear mixed modeling to assess the relationship between peritraumatic blood-based CpG methylation levels and CPTP. A total of 66 (27%) of the 248 CpG sites assessed in these models statistically significantly predicted CPTP, with the three most significantly associated CpG sites originating from the POMC gene region (ie, cg22900229 [β = .124, P < .001], cg16302441 [β = .443, P < .001], cg01926269 [β = .130, P < .001]). Among the genes analyzed, both POMC (z = 2.36, P = .018) and CRHBP (z = 4.89, P < .001) were enriched in CpG sites significantly associated with CPTP. Further, POMC expression was inversely correlated with methylation levels in a CPTP-dependent manner (6-months NRS<4: r = -.59, P < .001; 6-months NRS ≥ 4: r = -.18, P = .2312). Our results suggest that methylation of HPA axis genes including POMC and CRHBP predict risk for and may contribute to vulnerability to CPTP. PERSPECTIVE: Peritraumatic blood levels of CpG methylation sites in HPA axis genes, particularly CpG sites in the POMC gene, predict CPTP development. This data substantially advances our understanding of epigenetic predictors and potential mediators of CPTP, a highly common, morbid, and hard-to-treat form of chronic pain. - Source: PubMed
Publication date: 2023/03/10
Branham Erica MMcLean Samuel ADeliwala IshaniMauck Matthew CZhao YingMcKibben Lauren ALee AaronSpencer Alex BZannas Anthony SLechner MeganDanza TeresaVelilla Marc-AnthonyHendry Phyllis LPearson ClairePeak David AJones JeffreyRathlev Niels KLinnstaedt Sarah D - Suicide behavior (SB) has been highly associated with the response to stress and the hypothalamic-pituitary-adrenal (HPA) axis. The aim of this study was to summarize the results obtained in genetic studies that analyzed the HPA axis-stress pathway and SB through a systematic review. - Source: PubMed
Publication date: 2021/10/13
Hernández-Díaz YazmínGenis-Mendoza Alma DeliaGonzález-Castro Thelma BeatrizTovilla-Zárate Carlos AlfonsoJuárez-Rojop Isela EstherLópez-Narváez María LiliaNicolini Humberto