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The protein encoded by BCL2L14 belongs to the BCL2 protein family. Additionally we are shipping BCL2-Like 14 (Apoptosis Facilitator) Antibodies (36) and BCL2-Like 14 (Apoptosis Facilitator) Proteins (7) and many more products for this protein.
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Data indicate that LRP6 (show LRP6 ELISA Kits), BCL2L14, DUSP16 (show DUSP16 ELISA Kits), CREBL2 (show CREBL2 ELISA Kits), and CDKN1B (show CDKN1B ELISA Kits) were involed in centromeric (12p11.21-12p13.2) deletion in ETV6 (show ETV6 ELISA Kits)-RUNX1 (show RUNX1 ELISA Kits) B-cell precursor acute lymphoblastic leukemia (BCP (show OPN1SW ELISA Kits)-ALL).
Single nucleotide polymorphism in BCL2L14 is associated with lung cancer.
prior knockdown of Bcl-G expression ablates the stimulation of basal apoptosis by FAU (show FAU ELISA Kits), consistent with an essential downstream role for Bcl-G, itself a candidate tumour suppressor, in mediating the apoptosis regulatory role of FAU (show FAU ELISA Kits).
siRNA downregulation of Bcl-G inhibited breast cancer cell apoptosis. Adding an siRNA against Fau (show FAU ELISA Kits) revealed control of Bcl-G by Fau (show FAU ELISA Kits). The most important factors controlling Bcl-G are post-translational modification by Fau (show FAU ELISA Kits) & MELK (show MELK ELISA Kits), not transcription rate.
There was no somatic mutation of BH3 domains of Bad, Bmf (show BMF ELISA Kits) 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.
the kinase activity of MELK (show MELK ELISA Kits) is likely to affect mammary carcinogenesis through inhibition of the pro-apoptotic function of Bcl-GL
data presented here indicate that BH3 domain mutation of the proapoptotic genes Bad, Bmf (show BMF ELISA Kits) and Bcl-G is rare in laryngeal squamous cell carcinoma and may not contribute to the apoptosis-resistance mechanisms of laryngeal squamous cell carcinoma
JAB1 (show COPS5 ELISA Kits) is involved in the regulation of mitochondrial apoptotic pathway through specific interaction with BclGs.
Increased BclG(L) expression may contribute to the aberrant CD4 (show CD4 ELISA Kits)+ T cell apoptosis which causes an inappropriate immune response and impaired homeostasis in systemic lupus erythematosus.
CD3 (show CD3E ELISA Kits)/CD28 (show CD28 ELISA Kits)-inducible MNSFbeta (show FAU ELISA Kits)-Bcl-G complex may be involved in the regulation of T cell function and survival.
Bcl-G is expressed highly in mature spermatids in the testis, CD8 (show CD8A ELISA Kits)(+) conventional dendritic cells (DCs) in hematopoietic tissues and diverse epithelial cell types, including those lining the gastrointestinal and respiratory tracts.
The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. Overexpression of this gene has been shown to induce apoptosis in cells. Three alternatively spliced transcript variants encoding two distinct isoforms have been reported for this gene.
apoptosis facilitator Bcl-2-like protein 14
, apoptosis regulator BCL-G