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

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

1. Data indicate that LRP6 (zeige LRP6 Antikörper), BCL2L14, DUSP16 (zeige DUSP16 Antikörper), CREBL2 (zeige CREBL2 Antikörper), and CDKN1B (zeige CDKN1B Antikörper) were involed in centromeric (12p11.21-12p13.2) deletion in ETV6 (zeige ETV6 Antikörper)-RUNX1 (zeige RUNX1 Antikörper) B-cell precursor acute lymphoblastic leukemia (BCP (zeige OPN1SW Antikörper)-ALL).

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

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

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

5. There was no somatic mutation of BH3 domains of Bad, Bmf (zeige BMF Antikörper) 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.

6. the kinase activity of MELK (zeige MELK Antikörper) is likely to affect mammary carcinogenesis through inhibition of the pro-apoptotic function of Bcl-GL

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

8. JAB1 (zeige COPS5 Antikörper) is involved in the regulation of mitochondrial apoptotic pathway through specific interaction with BclGs.

9. Increased BclG(L) expression may contribute to the aberrant CD4 (zeige CD4 Antikörper)+ 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 (zeige CD3E Antikörper)/CD28 (zeige CD28 Antikörper)-inducible MNSFbeta (zeige FAU Antikörper)-Bcl-G complex may be involved in the regulation of T cell function and survival.

2. Bcl-G is expressed highly in mature spermatids in the testis, CD8 (zeige CD8A Antikörper)(+) conventional dendritic cells (DCs) in hematopoietic tissues and diverse epithelial cell types, including those lining the gastrointestinal and respiratory tracts.