anti-Angiotensin II Receptor-Associated Protein (AGTRAP) Antikörper

Human Angiotensin II Receptor-Associated Protein (AGTRAP) Interaktionspartner

1. A role for AT1 receptor-associated proteins in blood pressure regulation

2. ATRAP, a directly interacting and functionally inhibiting molecule of AT1R (zeige AGTR1 Antikörper), plays a protective role against the development of systemic insulin (zeige INS Antikörper) resistance via regulatory effects on adipose tissue function.

3. The phosphatidylinositol transfer protein (zeige PITPNA Antikörper) RdgBbeta (zeige PITPNC1 Antikörper) binds 14-3-3 (zeige YWHAQ Antikörper) via its unstructured C-terminus, whereas its lipid-binding domain interacts with the integral membrane protein ATRAP (angiotensin II type I receptor-associated protein).

4. the GG genotype of the AGTRAP rs11121816 T/G single nucleotide polymorphism was associated with increased mortality in two cohorts of patients who had septic shock.

5. CSF (zeige CSF2 Antikörper) angiotensin II, ACE (zeige ACE Antikörper), and ACE2 (zeige ACE2 Antikörper) levels are decreased in neuromyelitis optica/NMO spectrum disorder patients with anti-AQP4 (zeige AQP4 Antikörper) antibody, reflecting severe destruction of perivascular astrocytes

6. Small interfering RNA significantly attenuates angiotensin II type 1 receptor (zeige AGTR1 Antikörper)-stimulated inositol phosphate formation.

7. cloned a new human gene cDNA that codes for a homolog of the murine Agtrap protein

8. isolation of a novel protein, ARAP1 (zeige ARAP1 Antikörper), which promotes recycling of angiotensin(1A) to the plasma membrane in HEK (zeige EPHA3 Antikörper)-293 cells

9. CAML (zeige CAMLG Antikörper) is an important signal transducer for the actions of Ang II (zeige AGT Antikörper) in regulating the calcineurin-NFAT (zeige NFATC1 Antikörper) pathway and the interaction of CAML (zeige CAMLG Antikörper) with ATRAP may mediate the Ang II (zeige AGT Antikörper) actions in vascular physiology

Mouse (Murine) Angiotensin II Receptor-Associated Protein (AGTRAP) Interaktionspartner

1. Results presented in this study suggested that the enhancement in adipose ATRAP plays a protective role against the development of diet-induced visceral obesity and insulin (zeige INS Antikörper) resistance through improvement of adipose inflammation and function via the suppression of overactivation of adipose AT1R signaling.

2. Renal ATRAP downregulation is involved in the onset and progression of blood pressure elevation caused by renal mass reduction, and implicates ATRAP as a therapeutic target for hypertension in chronic kidney disease.

3. These results implied that AngII could effectively induce EpiCs to differentiate into vascular smooth muscle-like cells through the AT1 receptor.

4. ATRAP expression in brown adipose tissue does not influence the pathogenesis of dietary obesity or metabolic disorders.

5. Identify Atrap as a novel regulatory protein (zeige TGFB1 Antikörper) of the cardiac Ca(2+)-ATPase SERCA2a (zeige CA-P60A Antikörper). Suggest that Atrap enhances the activity of SERCA2a (zeige ATP2A2 Antikörper) and, consequently, facilitates ventricular relaxation.

6. These results suggest that increased formation of AT1R-P2Y6R (zeige P2RY6 Antikörper) heterodimers with age may increase the likelihood of hypertension induced by Ang II (zeige AGT Antikörper).

7. although erythropoiesis and blood pressure are negatively controlled through the AT1 receptor inhibition in vivo, the pathways involved are complex and distinct

8. Distal tubule-dominant enhancement of ATRAP inhibits pathological renal sodium reabsorption and blood pressure elevation in response to high salt loading.

9. AT1R knockout mice were less vulnerable to controlled cortical impact-induced injury.

10. The inhibition of degradation of angiotensin II type 1 receptor (zeige AGTR1 Antikörper)-associated protein (zeige BCAP31 Antikörper) (ATRAP) and inactivation of AT1R-mediated p38 MAPK (zeige MAPK14 Antikörper) and STAT3 (zeige STAT3 Antikörper) signaling pathways, are involved cardiac hypertrophy.