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PMID:23152932

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Citation

Yu, M, Gong, D, Lim, M, Arutyunyan, A, Groffen, J and Heisterkamp, N (2012) Lack of bcr and abr promotes hypoxia-induced pulmonary hypertension in mice. PLoS ONE 7:e49756

Abstract

Bcr and Abr are GTPase activating proteins that specifically downregulate activity of the small GTPase Rac in restricted cell types in vivo. Rac1 is expressed in smooth muscle cells, a critical cell type involved in the pathogenesis of pulmonary hypertension. The molecular mechanisms that underlie hypoxia-associated pulmonary hypertension are not well-defined.

Links

PubMed Online version:10.1371/journal.pone.0049756

Keywords


Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

MOUSE:BCR

involved_in

GO:0060313: negative regulation of blood vessel remodeling

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:BCR

involved_in

GO:0002692: negative regulation of cellular extravasation

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:BCR

GO:0060313: negative regulation of blood vessel remodeling

ECO:0000315:

P

Figure 2A shows that the walls of the pulmonary arteries of the bcr-/- mice are remarkably thicker than those of the wt mice after hypoxia, suggesting that bcr is one component needed for the prevention of artery remodeling

complete
CACAO 6049

MOUSE:BCR

GO:0043114: regulation of vascular permeability

ECO:0000315:

P

"Figure 3C shows that chronic hypoxia promoted loss of endothelial barrier function and, moreover, mice lacking Bcr...were clearly more severely affected." This suggests that bcr is a component needed for the prevention of vascular leakage under hypoxic conditions.

complete
CACAO 6056

MOUSE:BCR

GO:0002692: negative regulation of cellular extravasation

ECO:0000315:

P

Figure 3A shows that "pulmonary extravasation of leukocytes under hypoxia was significantly increased in the mice lacking... Bcr function as compared to wt mice," suggesting that bcr prevents leukocytes from pulmonary extravasation.

complete
CACAO 6069

MOUSE:BCR

involved_in

GO:0043114: regulation of vascular permeability

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:ABR

GO:0060313: negative regulation of blood vessel remodeling

ECO:0000315:

P

Figure 2A shows that the walls of the pulmonary arteries of the abr-/- mice are remarkably thicker than those of the wt mice after hypoxia, suggesting that abr is one component needed for the prevention of artery remodeling

complete
CACAO 6053

MOUSE:ABR

GO:0043114: regulation of vascular permeability

ECO:0000315:

P

"Figure 3C shows that chronic hypoxia promoted loss of endothelial barrier function and, moreover, mice lacking Abr...were clearly more severely affected." This suggests that abr is a component needed for the prevention of vascular leakage under hypoxic conditions.

complete
CACAO 6055

MOUSE:ABR

GO:0002692: negative regulation of cellular extravasation

ECO:0000315:

P

Figure 3A shows that "pulmonary extravasation of leukocytes under hypoxia was significantly increased in the mice lacking Abr...function as compared to wt mice," suggesting that abr prevents leukocytes from pulmonary extravasation.

complete
CACAO 6068

MOUSE:ABR

involved_in

GO:0060313: negative regulation of blood vessel remodeling

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:ABR

involved_in

GO:0043114: regulation of vascular permeability

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:ABR

involved_in

GO:0002692: negative regulation of cellular extravasation

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete


See also

References

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