CARMIL2 Monoclonal / Unconjugated / EM-53
Product Details
Description | RLTPR / CARMIL2 (RGD motif, leucine rich repeats, tropomodulin domain and proline-rich containing; capping protein regulator and myosin 1 linker 2), also known as LRRC16C, is a cytosolic protein, which with high affinity binds CAPZA2 (capping protein muscle actin Z-line alpha 2) and decreases CAPZA2 affinity for actin barbed ends. RLTPR / CARMIL2 increases the rate of actin filament elongation from seeds in the presence of CAPZA2, however, seems unable to nucleate filaments. Its interaction with CAPZA2 is essential for lamellipodial protrusion and cell translocation. RLTPR / CARMIL2 is crutial for T cell costimulation via CD28 and this property seems to be independent on its actin-uncapping function. The lack of functional RLTPR / CARMIL2 molecules impeded the differentiation toward Th1 and Th17 fates of both human and murine CD4+ T cells and leads to combined immunodeficiency. Expression of RLTPR / CARMIL2 was also detected in human and murine B cells, but it seems not to be involved in BCR-mediated signaling. | |
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Conjugate | Unconjugated | |
Clone | EM-53 | |
Target Species | Human, Mouse | |
Applications | FC, WB | |
Supplier | EXBIO | |
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About CARMIL2
This gene encodes a member of the CARMIL (capping protein, Arp2/3, myosin-I linker) family of proteins. The encoded protein interacts with and negatively regulates the heterodimeric capping protein and promotes cell migration. Reduced expression of this gene has been observed in human psoriasis patients. Mutations in this gene cause a human immunodeficiency syndrome characterized by smooth muscle tumors and impaired T-cell function. [provided by RefSeq, May 2017]
This gene encodes a member of the CARMIL (capping protein, Arp2/3, myosin-I linker) family of proteins. The encoded protein interacts with and negatively regulates the heterodimeric capping protein and promotes cell migration. Reduced expression of this gene has been observed in human psoriasis patients. Mutations in this gene cause a human immunodeficiency syndrome characterized by smooth muscle tumors and impaired T-cell function. [provided by RefSeq, May 2017]
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