CIDeRplusGeneral Information:
| Id: | 9,551 |
| Diseases: |
Cardiovascular disease
|
| Mus musculus | |
| Vav2-/- mouse | |
| article | |
| Reference: | Sauzeau V et al.(2007) Loss of Vav2 proto-oncogene causes tachycardia and cardiovascular disease in mice Mol. Biol. Cell 18: 943-952 [PMID: 17202406] |
Interaction Information:
| Comment | Loss of Vav2 proto-oncogene causes tachycardia and cardiovascular disease in mice. |
|
Formal Description Interaction-ID: 101246 |
|
| Comment | The Vav family is a group of signal transduction molecules that activate Rho/Rac GTPases during cell signaling. Experiments using knockout mice have indicated that the three Vav proteins present in mammals (Vav1, Vav2, and Vav3) are essential for proper signaling responses in hematopoietic cells. However, Vav2 and Vav3 are also highly expressed in non-hematopoietic tissues, suggesting that they may have additional functions outside blood cells. The disruption of the VAV2 locus in mice causes tachycardia, hypertension, and defects in the heart, arterial walls, and kidneys. |
|
Formal Description Interaction-ID: 101264 |
|
| Comment | The Vav family is a group of signal transduction molecules that activate Rho/Rac GTPases during cell signaling. Experiments using knockout mice have indicated that the three Vav proteins present in mammals (Vav1, Vav2, and Vav3) are essential for proper signaling responses in hematopoietic cells. However, Vav2 and Vav3 are also highly expressed in non-hematopoietic tissues, suggesting that they may have additional functions outside blood cells. The disruption of the VAV2 locus in mice causes tachycardia, hypertension, and defects in the heart, arterial walls, and kidneys. |
|
Formal Description Interaction-ID: 101266 |
|
| Comment | The hypertensive condition of Vav2-deficient mice is due to a chronic stimulation of the renin/angiotensin II and sympathetic nervous systems. |
|
Formal Description Interaction-ID: 101267 |
|
| Comment | Vav2-/- animals had extensive cardiovascular remodeling. |
|
Formal Description Interaction-ID: 101270 |
|
| Comment | Vav2-/- mice had enlarged heart left ventricles due to cardiomyocyte hypertrophy. The heart left ventricles were also fibrotic. No alterations were observed in the heart right ventricles. |
|
Formal Description Interaction-ID: 101272 |
|
| Comment | Vav2-/- mice had enlarged heart left ventricles due to cardiomyocyte hypertrophy. The heart left ventricles were also fibrotic. No alterations were observed in the heart right ventricles. |
|
Formal Description Interaction-ID: 101273 |
|
| Comment | The analysis of Vav2-/- mice evidenced defects in kidney function, including fibrosis and lower levels of urination, glomerular filtration, Na+ excretion,and creatinine clearance. |
|
Formal Description Interaction-ID: 101274 |
|
| Comment | No changes in the rates of K+ and Cl- excretion were found in Vav2-/- mice. Consistent with these results, the plasma of Vav2-/- mice contained high levels of vasopressin and aldosterone, the hormones regulating water and Na+ reabsorption in nephrons, respectively. |
|
Formal Description Interaction-ID: 101275 |
|
| Comment | No changes in the rates of K+ and Cl- excretion were found in Vav2-/- mice. Consistent with these results, the plasma of Vav2-/- mice contained high levels of vasopressin and aldosterone, the hormones regulating water and Na+ reabsorption in nephrons, respectively. |
|
Formal Description Interaction-ID: 101276 |
|
| Drugbank entries | Show/Hide entries for |
| Comment | High levels of angiotensin II (AngII) and reduced bradykinin concentrations were found in the plasma of Vav2null mice. |
|
Formal Description Interaction-ID: 101277 |
|
| Comment | High levels of angiotensin II (AngII) and reduced bradykinin concentrations were found in the plasma of Vav2null mice. |
|
Formal Description Interaction-ID: 101278 |
|
| Comment | The mRNA encoding the angiotensin II (AngII) AT1 receptor involved in vasoconstriction responses was up-regulated in the aorta and hearts of Vav2-/- mice. |
|
Formal Description Interaction-ID: 101279 |
|
| Drugbank entries | Show/Hide entries for AGTR1 |
| Comment | High levels of both renin and ACE were observed in Vav2-/- mice. |
|
Formal Description Interaction-ID: 101280 |
|
| Drugbank entries | Show/Hide entries for REN |
| Comment | High levels of both renin and ACE were observed in Vav2-/- mice. |
|
Formal Description Interaction-ID: 101281 |
|
| Drugbank entries | Show/Hide entries for ACE |
| Comment | The sympathetic nervous system (SNS) regulates the cardiovascular system by influencing heart rate, cardiac contraction, vascular tone, and renin r-lease. In addition, it promotes water reabsorption in kidneys by inducing vasopressin release from the pituitary gland. The action of the SNS on the cardiovascular system is mediated by two catecholamines: adrenaline and noradrenaline. The plasma concentrations of noradrenaline and adrenaline but not of dopamine, were elevated in Vav2-/- mice. |
|
Formal Description Interaction-ID: 101282 |
|
| Comment | The sympathetic nervous system (SNS) regulates the cardiovascular system by influencing heart rate, cardiac contraction, vascular tone, and renin r-lease. In addition, it promotes water reabsorption in kidneys by inducing vasopressin release from the pituitary gland. The action of the SNS on the cardiovascular system is mediated by two catecholamines: adrenaline and noradrenaline. The plasma concentrations of noradrenaline and adrenaline but not of dopamine, were elevated in Vav2-/- mice. |
|
Formal Description Interaction-ID: 101283 |
|