Introduction of LAPTM5
LAPTM5, the full protein name being lysosomal-associated transmembrane protein 5, is encoded by the LAPTM5 gene in humans. The gene encodes a transmembrane receptor which is associated with lysosomes. The encoded protein, also known as E3 protein, may play a role in hematopoiesis. It’s broadly expressed in bone marrow, lymph node and 15 other tissues. It may have a special functional role during embryogenesis and in adult hematopoietic cells.
|Basic Information of LAPTM5|
|Protein Name||Lysosomal-associated transmembrane protein 5|
|Aliases||Lysosomal-associated multitransmembrane protein 5, Retinoic acid-inducible E3 protein, KIAA0085|
|Organism||Homo sapiens (Human)|
Function of LAPTM5 Membrane Protein
LAPTM5 (lysosomal-associated protein transmembrane 5) is preferentially expressed in immune cells, which is also known as KIAA0085, and it can interact with the Nedd4 family of ubiquitin ligases. It has been reported that LAPTM5 acts as a positive regulator of inflammatory signaling pathways and cytokine secretion in macrophages. Also, LAPTM5 can negatively regulate TCR expression and T cell activation by promoting CD3ζ degradation in lysosomes. In addition, LAPTM5 may contribute to tumorigenesis in a subset of human cancers. Some publications have indicated that LAPTM5 is related with cell proliferation and viability by G0/G1 cell cycle arrest. Moreover, it may have a special functional role during embryogenesis and in adult hematopoietic cells. LAPTM5 is overexpressed in HeLa cells, and it can induce apoptosis via cleavage of Mcl-1 and Bid via a LAPTM5-associated lysosomal pathway, and the following activation of the mitochondria-dependent caspase cascade. Furthermore, LAPTM5 may contribute to tumorigenesis in different kinds of human cancers.
Fig.1 Model of the relationship between LAPTM5-mediated degeneration and propensity for spontaneous regression of NB tumor (Inoue, 2009)
Application of LAPTM5 Membrane Protein in Literature
This article demonstrates that LAPTM5 is overexpressed in HeLa cells which induce apoptosis via cleavage of Mcl-1 and Bid by a LAPTM5-associated lysosomal pathway, and subsequent activation of the mitochondria-dependent caspase cascade.
This article shows that downregulated LAPTM5 suppresses proliferation and viability, also induces G0/G1 cell cycle arrest, possibly via deactivation of ERK1/2 and p38 in BCa cells.
This study suggests that LAPTM5 deficiency may contribute to tumorigenesis in different subsets of human cancers.
This article demonstrates that low expression of LAPTM5 may take part in the pathogenesis of SLE and contribute to the severity of the disease. In a Chinese population, none of LAPTM5 polymorphisms contributes significantly to SLE susceptibility.
This article indicates that CD3ζ can be degraded by two pathways: one is SLAP/c-Cbl, which targets internalized cell surface CD3ζ, and the other is LAPTM5, which targets intracellular CD3ζ.
LAPTM5 Preparation Options
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