anti-Lysosomal Protein Transmembrane 5 (LAPTM5) Antibodies

Human Lysosomal Protein Transmembrane 5 (LAPTM5) interaction partners

1. These findings suggest that the inactivation of LAPTM5 may contribute to tumorigenesis in a subset of human cancers

2. Taken together, our results suggested that decreased LAPTM5 inhibited proliferation and viability, as well as induced G0/G1 cell cycle arrest possibly via deactivation of ERK1/2 and p38 in BCa cells

3. Insufficient expression of LAPTM5 may take part in the pathogenesis of systemic lupus erythematosus (SLE) and contribute to the severity of the disease, none of LAPTM5 polymorphisms contributes significantly to SLE susceptibility in a Chinese population.

4. The interaction of LAPTM5 with CD1e and their colocalization in antigen processing compartments both suggest that LAPTM5 might influence the role of CD1e in the presentation of lipid antigens.

5. LAPTM5 is a substrate of the ITCH-mediated degradation and its protein level is negatively regulated by ITCH

6. LAPTM5-mediated programmed cell death is closely associated with the spontaneous regression of neuroblastomas

7. LAPTM5 shows stage-specific expression during B cell differentiation. It may be involved in B cell malignancies.

8. results suggest that loss of E3 gene expression might be a crucial event during the progression of human MM

Mouse (Murine) Lysosomal Protein Transmembrane 5 (LAPTM5) interaction partners

1. these results suggest that CD3zeta can be degraded by two pathways: SLAP/c-Cbl, which targets internalized cell surface CD3zeta dependent on TCR signaling, and LAPTM5, which targets intracellular CD3zeta independent of TCR signaling.

2. the pre-BCR induces the downmodulation of its own expression through induction of LAPTM5, which promotes the lysosomal transport and degradation of the intracellular pre-BCR pool and limits the supply of pre-BCR to the cell surface

3. LAPTM5 acts as a positive modulator of inflammatory signaling pathways and hence cytokine secretion in macrophages

4. LAPTM5 physically interacts with the B cell receptor complex and promotes its degradation in the lysosomal compartment in mouse B cells.

5. the lysosomal protein LAPTM5 negatively regulated surface TCR expression by specifically interacting with the invariant signal-transducing CD3zeta chain and promoting its degradation