核纤层蛋白B2重组兔单抗

LMNB2

Lamin-B2

Interacts with TMEM43 (By similarity).

Nucleus inner membrane; Lipid-anchor; Nucleoplasmic side.

B-type lamins undergo a series of modifications, such as farnesylation and phosphorylation. Increased phosphorylation of the lamins occurs before envelope disintegration and probably plays a role in regulating lamin associations.

Defects in LMNB2 are a cause of partial acquired lipodystrophy (APLD) [MIM:608709]. A rare childhood disease characterized by loss of subcutaneous fat from the face and trunk. Fat deposition on the pelvic girdle and lower limbs is normal or excessive. Most frequently, onset between 5 and 15 years of age. Most affected subjects are females and some show no other abnormality, but many develop glomerulonephritis, diabetes mellitus, hyperlipidemia, and complement deficiency. Mental retardation in some cases. APLD is a sporadic disorder of unknown etiology.

Belongs to the intermediate filament family.

Lamins are components of the nuclear lamina, a fibrous layer on the nucleoplasmic side of the inner nuclear membrane, which is thought to provide a framework for the nuclear envelope and may also interact with chromatin.