| First Author | Chen L | Year | 2009 |
| Journal | J Biol Chem | Volume | 284 |
| Issue | 40 | Pages | 27409-15 |
| PubMed ID | 19654325 | Mgi Jnum | J:156352 |
| Mgi Id | MGI:4420368 | Doi | 10.1074/jbc.M109.025460 |
| Citation | Chen L, et al. (2009) Suppression of tumor angiogenesis by Galpha(13) haploinsufficiency. J Biol Chem 284(40):27409-15 |
| abstractText | Heterotrimeric G proteins are critical transducers of cellular signaling. Of the four families of G proteins, the physiological function of Galpha(13) is less well understood. Galpha(13) gene-deleted mice die at embryonic day approximately 9.5. Here, we show that heterozygous Galpha(13)(+/-) mice display defects in adult angiogenesis. Female Galpha(13)(+/-) mice showed a higher number of immature follicles and a lower density of blood vessels in the mature corpus luteum compared with Galpha(13)(+/+) mice. Furthermore, implanted tumors grew slower in Galpha(13)(+/-) host mice. These tumor tissues had many fewer blood vessels compared with those from Galpha(13)(+/+) host mice. Moreover, bone marrow-derived progenitor cells from Galpha(13)(+/+) mice rescued the failed growth of allografted tumors when reconstituted into irradiated Galpha(13)(+/-) mice. Hence, Galpha(13) is haploinsufficient for adult angiogenesis in both the female reproductive system and tumor angiogenesis. |
