| dc.contributor.author | Majumder, Syamantak | |
| dc.date.accessioned | 2021-10-02T17:50:05Z | |
| dc.date.available | 2021-10-02T17:50:05Z | |
| dc.date.issued | 2009-11-30 | |
| dc.identifier.uri | https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/j.1476-5381.2009.00446.x | |
| dc.identifier.uri | http://dspace.bits-pilani.ac.in:8080/xmlui/handle/123456789/2440 | |
| dc.description.abstract | Nitric oxide (NO) promotes angiogenesis by activating endothelial cells. Thalidomide arrests angiogenesis by interacting with the NO pathway, but its putative targets are not known. Here, we have attempted to identify these targets | en_US |
| dc.language.iso | en | en_US |
| dc.publisher | Wiley | en_US |
| dc.subject | Biology | en_US |
| dc.subject | Thalidomide | en_US |
| dc.subject | Nitric oxide-driven | en_US |
| dc.subject | Guanylyl cyclase | en_US |
| dc.title | Thalidomide attenuates nitric oxide-driven angiogenesis by interacting with soluble guanylyl cyclase | en_US |
| dc.type | Article | en_US |
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