High impact information on CR1L

• Units of duplication range from single SCRs, to septamers such as efbkdaj, to extensive segments such as MCP-CR1L [1].
• This study examines the effects of duplication and insertions-deletions (indels) by comparing human complement receptor 1 (CR1) and human CR1-like (CR1L) with syntenic genes from four other vertebrates (chimpanzee, baboon, rat, and mouse) [2].
• However, northern blot analysis of various other lymphoid tissue identified a candidate CR1L transcript in human fetal liver [3].
• Expression in COS-7 cells yielded a human CR1L protein of approximately 50 kDa that exhibited binding specificity for iC4 but not for iC3 [3].
• Neither northern nor western blot analysis of human bone marrow revealed the presence of the CR1L transcript or protein [3].

Biological context of CR1L

• Human CR1L was previously identified from genomic clones that predict exons for seven SCRs, and there have been no reports of CR1L expression [3].

Anatomical context of CR1L

• Thus, expression of the CR1L transcript appears to be limited to hematopoietic and fetal lymphoid tissue [3].
• PCR amplification of a cDNA panel of human fetal tissue confirmed the presence of the CR1L transcript in fetal liver, and to a lesser extent in fetal spleen and thymus [3].

Other interactions of CR1L

• The degeneration of the g SCR must have occurred prior to the formation of primate CR1L and prior to the duplication events which resulted in primate CR1 [4].
• The first 6.5 SCRs matched 100% with the predicted human CR1L sequence, while the second half of SCR 7 was homologous to the comparable chimp CR1L sequence but with a stop codon [3].

References