anti-BCL2-Like 14 (Apoptosis Facilitator) (BCL2L14) Antikörper

Human BCL2-Like 14 (Apoptosis Facilitator) (BCL2L14) Interaktionspartner

1. BCL2L14 knockdown exhibited similar effects similar to those of miR-496 overexpression, and the restored BCL2L14expression reversed the protective effects of miR-496 on SH-SY5Y cells

2. The results show that BCLG is overexpressed more frequently in medullary breast carcinoma than other histological types of basal like carcinomas.

3. Data indicate that LRP6, BCL2L14, DUSP16, CREBL2, and CDKN1B were involed in centromeric (12p11.21-12p13.2) deletion in ETV6-RUNX1 B-cell precursor acute lymphoblastic leukemia (BCP-ALL).

4. Single nucleotide polymorphism in BCL2L14 is associated with lung cancer.

5. prior knockdown of Bcl-G expression ablates the stimulation of basal apoptosis by FAU, consistent with an essential downstream role for Bcl-G, itself a candidate tumour suppressor, in mediating the apoptosis regulatory role of FAU.

6. siRNA downregulation of Bcl-G inhibited breast cancer cell apoptosis. Adding an siRNA against Fau revealed control of Bcl-G by Fau. The most important factors controlling Bcl-G are post-translational modification by Fau & MELK, not transcription rate.

7. There was no somatic mutation of BH3 domains of Bad, Bmf and Bcl-G genes in transitional cell carcinoma samples. The data presented here indicate that BH3 domain mutation of these genes is rare in TCCs and may not contribute to the pathogenesis of TCCs.

8. the kinase activity of MELK is likely to affect mammary carcinogenesis through inhibition of the pro-apoptotic function of Bcl-GL

9. data presented here indicate that BH3 domain mutation of the proapoptotic genes Bad, Bmf and Bcl-G is rare in laryngeal squamous cell carcinoma and may not contribute to the apoptosis-resistance mechanisms of laryngeal squamous cell carcinoma

10. JAB1 is involved in the regulation of mitochondrial apoptotic pathway through specific interaction with BclGs.

11. Increased BclG(L) expression may contribute to the aberrant CD4+ T cell apoptosis which causes an inappropriate immune response and impaired homeostasis in systemic lupus erythematosus.

Mouse (Murine) BCL2-Like 14 (Apoptosis Facilitator) (BCL2L14) Interaktionspartner

1. CD3/CD28-inducible MNSFbeta-Bcl-G complex may be involved in the regulation of T cell function and survival.

2. The Bcl-G interacts specifically with proteins of the transport particle protein complex.

3. Bcl-G is expressed highly in mature spermatids in the testis, CD8(+) conventional dendritic cells (DCs) in hematopoietic tissues and diverse epithelial cell types, including those lining the gastrointestinal and respiratory tracts.