Thalidomide attenuates nitric oxide-driven angiogenesis by interacting with soluble guanylyl cyclase

dc.contributor.authorMajumder, Syamantak
dc.date.accessioned2021-10-02T17:50:05Z
dc.date.available2021-10-02T17:50:05Z
dc.date.issued2009-11-30
dc.description.abstractNitric 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 targetsen_US
dc.identifier.urihttps://bpspubs.onlinelibrary.wiley.com/doi/10.1111/j.1476-5381.2009.00446.x
dc.identifier.urihttp://dspace.bits-pilani.ac.in:8080/xmlui/handle/123456789/2440
dc.language.isoenen_US
dc.publisherWileyen_US
dc.subjectBiologyen_US
dc.subjectThalidomideen_US
dc.subjectNitric oxide-drivenen_US
dc.subjectGuanylyl cyclaseen_US
dc.titleThalidomide attenuates nitric oxide-driven angiogenesis by interacting with soluble guanylyl cyclaseen_US
dc.typeArticleen_US

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