Recombinant Human MBL Protein

重组人MBL蛋白 | 重组人甘露糖结合凝集素蛋白

COLEC1 | COLEC1collectin-1 | Collectin-1 | HSMBPC | Mannan-binding protein | mannose-binding lectin (protein C) 2, soluble (opsonic defect) | mannose-binding lectin (protein C) 2, soluble | Mannose-binding lectin | mannose-binding protein C | MBL | MBL2 |

rp181609-10μg

10μg

无动物源

≥90%(SDS-PAGE)

MBL (mannose-binding lectin) is primarily a liver-derived collagen-like serum protein, which binds sugar structures on micro-organisms and dying host cells and is one of the four known mediators that initiate activation of the complement system via the lectin pathway. MBL and the ficolins (Ficolin-1, Ficolin-2, and Ficolin-3) are soluble collagen-like proteins that are involved in innate immune defense. They bind sugar structures or acetylated compounds present on microorganisms and dying host cells and they initiate activation of the lectin complement pathway in varying degrees. MBL2 encodes the mannose-binding lectin, which is a key player in the innate immune system and has recently been found to play a role in the development of type 1 diabetes and gestational diabetes mellitus. Common variant alleles situated both in the promoter and structural regions of the MBL2 gene influence the stability and the serum concentration of the protein. Several polymorphisms in the promoter and structural regions of MBL2 adversely affect the plasma concentration and the oligomeric state of MBL. The possession of mutant alleles has been linked to disease outcomes for a variety of bacterial and viral infections. Mutant MBL2 haplotypes have been linked to disease progression and response to therapy in HCV infection.

Testing in progress

重组表达

24.8 kDa

C-His

29.3 & 51.4 kDa, under reducing conditions; 51.4 & 89.8 & 124.6 & 210.6 kDa, under non-reducing conditions.

CHO Accession #: P11226 | CHO

<1.0 EU/μg

人(Human)

1-248 aa

MSLFPSLPLLLLSMVAASYSETVTCEDAQKTCPAVIACSSPGINGFPGKDGRDGTKGEKGEPGQGLRGLQGPPGKLGPPGNPGPSGSPGPKGQKGDPGKSPDGDSSLAASERKALQTEMARIKKWLTFSLGKQVGNKFFLTNGEIMTFEKVKALCVKFQASVATPRNAAENGAIQNLIKEEAFLGITDEKTEGQFVDLTGNRLTYTNWNEGEPNNAGSDEDCVLLLKNGQWNDVPCSTSHLAVCEFPIHHHHHH

Yes

Yes