High impact information on Rgs1

• These results demonstrate opposing roles for Rgs1 and Gnai2 in B cell trafficking into and within lymph nodes [1].
• Intravital microscopy of adoptively transferred B cells from wild-type and Rgs1-/- mice revealed that Rgs1-/- B cells stick better to lymph node high endothelial venules, home better to lymph nodes, and move more rapidly within lymph node follicles than do wild-type B cells [1].
• Many of the B-cell follicles in the spleens of Rgs1(-/-) mice have germinal centers even in the absence of immune stimulation [2].
• Abnormal B-cell responses to chemokines, disturbed plasma cell localization, and distorted immune tissue architecture in Rgs1-/- mice [2].
• Here we show that Rgs1(-/-) mice possess B cells that respond excessively and desensitize improperly to the chemokines CXCL12 and CXCL13 [2].

Biological context of Rgs1

• CD40 signaling, by contrast, fails to cause rapid up-regulation of RGS1 or RGS2 [3].

Anatomical context of Rgs1

• RGS1, RGS2 and RGS16, other members of the R4 subfamily, were expressed in distinct progenitor and mature myeloerythroid and lymphoid lineage blood cells [4].
• Our results show an inverse correlation between the capacity to migrate and the levels of RGS1, RGS9 and RGS16 for both naive and regulatory T cells [5].

Associations of Rgs1 with chemical compounds

• RGS16 was as effective as RGS1 in inhibiting carbachol-dependent signaling but only partially inhibited the response to CCK [6].

Physical interactions of Rgs1

• Anergic hen egg lysozyme autoantigen-binding B cells are also shown to have slightly elevated RGS1 and RGS2 expression [3].

Other interactions of Rgs1

• We present the sequence of mouse RGS1 and describe a novel short isoform of RGS3 that we term RGS3s [3].

References