p(MGI:Crh)

Entity

Name

Crh

Namespace

mgi

Namespace Version

20181021

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/f2f993e599694ab5ce989cc39d789a499f75db99/external/mgi-names.belns

Interestingly, the addition of a 10-fold excess of the CRH-R1 antagonist, antalarmin, overcame the negative effect of CRH on estradiol release (d 5, P 􏰄 0.009; d 7, P 􏰄 0.010; d 9, P 􏰃 0.001; and d 11, P 􏰄 0.002), indicating that the suppressive effect of CRH was receptor mediated (Fig. 1). PubMed:23211705

The addition of the CRH-R1 an- tagonist antalarmin in a 10-fold higher concentration compared with that of CRH overcame the effect of CRH on beta􏰇-hCG release (d 11 beta􏰇-hCG 185.6 􏰅 6.087 mIU/ml, P 􏰃 0.001) indicating that the suppressive effect of CRH was recep- tor mediated (Fig. 3). PubMed:23211705

The addition of a 10-fold excess of the CRH-R1 antagonist antalarmin reversed the negative ef- fect of CRH on progesterone release (d 11 progesterone 0.712 􏰅 0.004 ng/ml, P 􏰃 0.001), suggesting that the suppressive effect of CRH was receptor mediated (Fig. 2). PubMed:23211705

The addition of the CRH-R1 an- tagonist antalarmin in a 10-fold higher concentration compared with that of CRH overcame the effect of CRH on 􏰇-hCG release (d 11 beta􏰇-hCG 185.6 􏰅 6.087 mIU/ml, P 􏰃 0.001) indicating that the suppressive effect of CRH was recep- tor mediated (Fig. 3). PubMed:23211705

The addition of the CRH-R1 an- tagonist antalarmin in a 10-fold higher concentration compared with that of CRH overcame the effect of CRH on 􏰇-hCG release (d 11 beta􏰇-hCG 185.6 􏰅 6.087 mIU/ml, P 􏰃 0.001) indicating that the suppressive effect of CRH was recep- tor mediated (Fig. 3). PubMed:23211705

CRF-OE mice had significantly elevated tau-P compared to wild type (WT) mice at the AT8 (S202/T204), PHF-1 (S396/404), S262, and S422 sites. Treating CRF-OE mice with R121919 blocked phosphorylation at the AT8 (S202/T204) and PHF-1 (S396/404) sites, but not at the S262 and S422 sites and reduced phosphorylation of c-Jun N Terminal Kinase (JNK). PubMed:25125464

CRF-OE mice had significantly elevated tau-P compared to wild type (WT) mice at the AT8 (S202/T204), PHF-1 (S396/404), S262, and S422 sites. Treating CRF-OE mice with R121919 blocked phosphorylation at the AT8 (S202/T204) and PHF-1 (S396/404) sites, but not at the S262 and S422 sites and reduced phosphorylation of c-Jun N Terminal Kinase (JNK). PubMed:25125464

Interestingly, the addition of a 10-fold excess of the CRH-R1 antagonist, antalarmin, overcame the negative effect of CRH on estradiol release (d 5, P 􏰄 0.009; d 7, P 􏰄 0.010; d 9, P 􏰃 0.001; and d 11, P 􏰄 0.002), indicating that the suppressive effect of CRH was receptor mediated (Fig. 1). PubMed:23211705

The addition of the CRH-R1 an- tagonist antalarmin in a 10-fold higher concentration compared with that of CRH overcame the effect of CRH on beta􏰇-hCG release (d 11 beta􏰇-hCG 185.6 􏰅 6.087 mIU/ml, P 􏰃 0.001) indicating that the suppressive effect of CRH was recep- tor mediated (Fig. 3). PubMed:23211705

In the CRH 10􏰁7 mol/liter group, the amount of beta􏰇-hCG measured in the culture medium was elevated but to a lesser extent compared with the control group (d 11 􏰇-hCG 6.05 􏰅 0.077 mIU/ml, P 􏰃 0.001). PubMed:23211705

Notably, CRH did not affect the amount of progesterone released into the incubation medium up to d 9, whereas it suppressed pro- gesterone levels on d 11 (d 11 progesterone 0.030 􏰅 0.000 ng/ml, P 􏰃 0.001). PubMed:23211705

Notably, CRH did not affect the amount of progesterone released into the incubation medium up to d 9, whereas it suppressed pro- gesterone levels on d 11 (d 11 progesterone 0.030 􏰅 0.000 ng/ml, P 􏰃 0.001). PubMed:23211705

The addition of a 10-fold excess of the CRH-R1 antagonist antalarmin reversed the negative ef- fect of CRH on progesterone release (d 11 progesterone 0.712 􏰅 0.004 ng/ml, P 􏰃 0.001), suggesting that the suppressive effect of CRH was receptor mediated (Fig. 2). PubMed:23211705

CRF-OE mice had significantly elevated tau-P compared to wild type (WT) mice at the AT8 (S202/T204), PHF-1 (S396/404), S262, and S422 sites. Treating CRF-OE mice with R121919 blocked phosphorylation at the AT8 (S202/T204) and PHF-1 (S396/404) sites, but not at the S262 and S422 sites and reduced phosphorylation of c-Jun N Terminal Kinase (JNK). PubMed:25125464

CRF-OE mice had significantly elevated tau-P compared to wild type (WT) mice at the AT8 (S202/T204), PHF-1 (S396/404), S262, and S422 sites. Treating CRF-OE mice with R121919 blocked phosphorylation at the AT8 (S202/T204) and PHF-1 (S396/404) sites, but not at the S262 and S422 sites and reduced phosphorylation of c-Jun N Terminal Kinase (JNK). PubMed:25125464

CRF-OE mice had significantly elevated tau-P compared to wild type (WT) mice at the AT8 (S202/T204), PHF-1 (S396/404), S262, and S422 sites. Treating CRF-OE mice with R121919 blocked phosphorylation at the AT8 (S202/T204) and PHF-1 (S396/404) sites, but not at the S262 and S422 sites and reduced phosphorylation of c-Jun N Terminal Kinase (JNK). PubMed:25125464

CRF-OE mice had significantly elevated tau-P compared to wild type (WT) mice at the AT8 (S202/T204), PHF-1 (S396/404), S262, and S422 sites. Treating CRF-OE mice with R121919 blocked phosphorylation at the AT8 (S202/T204) and PHF-1 (S396/404) sites, but not at the S262 and S422 sites and reduced phosphorylation of c-Jun N Terminal Kinase (JNK). PubMed:25125464