BCL2L14 (BCL2-like 14 (apoptosis facilitator))

2013-08-01   Mark R Pickard  , Gwyn T Williams  

Institute of Science, Technology in Medicine, Keele University, Keele, United Kingdom

Identity

HGNC
LOCATION
12p13.2
LOCUSID
ALIAS
BCLG
FUSION GENES

DNA/RNA

Atlas Image
Figure 1. Alternative splicing of BCL2L14 yields at least three transcript variants. Note that exons only are drawn to scale and that only those transcript variants for which reference sequences exist are shown. Transcript variants 1 and 4 differ only in their 5-UTR sequence and produce an identical protein isoform (Bcl-GL), whereas the coding sequence of transcript variant 2 is shorter and gives rise to a protein isoform (Bcl-GS) with a distinct C-terminus.

Description

The gene is located on chromosome 12 on the plus strand at 12202778 bp from pter to 12364018 from pter (size is 161241 bases). It was originally thought to comprise 6 exons (Guo et al., 2001) but 7 possible additional exons have subsequently been identified (Montpetit et al., 2002).

Transcription

The gene encodes multiple transcripts; reference sequences exist for 3 transcript variants. These give rise to two different protein isoforms (Fig. 1). Transcript variants 1 and 4 differ only in their 5-UTR and both encode the same protein, termed isoform 1 or Bcl-GL. Usage of a different splice acceptor site results in the production of transcript variant 2. This contains extra nucleotides within the coding sequence, resulting in a frameshift and consequently a truncated protein product with distinct C-terminal amino acids, termed isoform 2 or Bcl-GS. Transcript variant 2 may be a candidate for nonsense-mediated mRNA decay (NMD), but the RefSeq record (NM_030766.1) has been retained, since there is evidence for the expression of protein product. However, the RefSeq (NM_138724.1) for a further variant, originally termed variant 3, which encodes Bcl-G-Median (Bcl-GM) (Montpetit et al., 2002), has been permanently suppressed, as this transcript is also a candidate for NMD and evidence for protein expression is lacking.

Pseudogene

There are no known pseudogenes.

Proteins

Atlas Image
Figure 2. Protein isoforms encoded by BCL2L14. Homologous sequence between the two isoforms is depicted by the same colour pattern. Note that BclGL contains BH2 and BH3 domains whereas BclGS is a BH3-only protein. Potential sites of post-translational modification/interaction with non-Bcl-2 family members are also indicated.

Description

The two protein isoforms are members of the Bcl-2 family. Bcl-GL comprises 327 amino acids and contains BH2 and BH3 domains, whereas Bcl-GS comprises 252 amino acids and contains the BH3 domain only (Fig. 2). The two proteins are identical in sequence for the first 226 amino acids.

Expression

Highest levels of gene expression in the adult human are found in testis, hence the name Bcl-G, for Bcl-Gonad. Indeed Bcl-GS is uniquely expressed in this tissue (as also noted for Bcl-GM) (Guo et al., 2001; Montpetit et al., 2002). Bcl-GL is predominantly expressed in testis, with transcripts also present in lung, pancreas, prostate, bone marrow and colon (Guo et al., 2001; Montpetit et al., 2002). The expression of Bcl-GL has also been reported in freshly isolated human T-lymphocytes (CD4+ and CD8+ cells) and B-lymphocytes (Luo et al., 2009). Both Bcl-GL and Bcl-GS transcripts are expressed in a wide range of breast cancer cell lines and cultured mammary epithelial cells, but protein expression has been demonstrated for the former isoform only (Benito et al., 2006; Lin et al., 2007). Bcl-G transcript expression is more variable across prostate cell lines (Pickard et al., 2010). High levels of Bcl-GS transcripts are found in testicular embryonal cancer cell lines, with lower levels present in urinary bladder and mantle cell lymphoma cell lines, followed by myeloid and breast cancer cell lines, but protein was detected for the testicular embryonal cancer cell lines only (Benito et al., 2006).

Localisation

Expression of GFP-tagged proteins in COS-7 cells has revealed a diffuse localization throughout the cell for Bcl-GL (similar to GFP alone), but a more punctate cytosolic localization, with partial co-localization to mitochondria, for Bcl-GS (Guo et al., 2001). The latter has been confirmed using Myc-tagged Bcl-GS (Liu et al., 2008). Deletion of the BH3 domain from Bcl-GS has no effect on its subcellular distribution, despite preventing interaction with Bcl-XL (Guo et al., 2001). However interaction with JAB1 results in a more diffuse cytoplasmic localisation for Bcl-GS (Liu et al., 2008).

Function

The original paper on BCL2L14 reported that GFP- or FLAG-tagged Bcl-GL and Bcl-GS have pro-apoptotic activity in a range of cell lines (COS-7, HEK293T and PC3), and that the latter is the more potent isoform (Guo et al., 2001). Deletion of the BH2 domain from Bcl-GL allowed its interaction with Bcl-XL and enhanced apoptotic activity, whereas the BH3 domain of Bcl-GS was required for interaction with Bcl-XL and apoptotic activity (Guo et al., 2001).
The pro-apoptotic activity of Bcl-GL in COS-7 cells has been independently confirmed, and it has been further demonstrated that this activity is negatively regulated by phosphorylation, catalyzed by MELK (Lin et al., 2007). Similarly, Bcl-GS has been reported to induce basal apoptosis in HeLa cells; an effect that is potentiated by JAB1 (Liu et al., 2008). The latter is thought to out-compete Bcl-2/Bcl-XL for binding of Bcl-GS (Liu et al., 2008). On the other hand, transfection of Huh-7 cells with Bcl-GL has no effect on basal apoptosis (Zhang et al., 2006), while the survival of HCT116 and NTERA2 cells is unaffected by elevated levels of Bcl-GS consequent upon ectopic TEF expression (Benito et al., 2006), suggesting that cell context is important for the apoptotic activity of Bcl-G protein isoforms. Crucially lentiviral transfection of Bcl-GL results in enhanced apoptosis of CD4+ T-cells from healthy subjects, demonstrating that pro-apoptotic activity is not restricted to transformed cells (Luo et al., 2009).
Furthermore, siRNA-mediated silencing of BCL2L14 gene expression attenuates apoptosis induction in several cell lines in response to diverse stimuli, including: ultraviolet-C irradiation (22Rv1 and HEK293T cells) (Pickard et al., 2010; Pickard et al., 2011), etoposide (HCT116 cells) (Benito et al., 2006), neratinib (SKBR-3 cells) (Seyhan et al., 2012), p53-induction (Saos-2 cells) (Miled et al., 2005), and ectopic expression of the putative tumour suppressor gene FAU (HEK293T cells) (Pickard et al., 2011). BCL2L14 is itself a target gene for the apoptosis master regulator p53 (Miled et al., 2005), and it is one of a subset of pro-apoptotic genes whose expression is hyperactivated in response to interferon-α and -γ co-treatment of hepatoma cells (Zhang et al., 2006). Its expression is also increased in mammalian cells following exposure to a diverse range of apoptotic stimuli (including chemotherapeutic agents) such as: gamma- radiation therapy (Finnberg et al., 2008), UV-C irradiation (Pickard et al., 2011), arsenic trioxide (Galimberti et al., 2012), nanoparticulate tetraiodothyroacetic acid (Glinskii et al., 2009), etoposide and cisplatin (Benito et al., 2006).
Mutations in pancreatic/duodenum homeobox protein 1 (PDX1) can result in human type 2 diabetes. Haploinsufficiency of this gene in mice also causes diabetes and is associated with enhanced apoptosis/necrosis of β-cells. In this regard, BCL2L14 has been identified as one of several genes encoding pro-apoptotic Bcl-2 family members whose expression is markedly up-regulated following shRNA-mediated depletion of Pdx1 in mouse insulinoma MIN6 cells (Fujimoto et al., 2010). Additionally BCL2L14 is one of several pro-apoptotic genes that is up-regulated upon exposure of human fibroblasts to pressure-induced oxidative stress (Oh et al., 2008).
The recent production of a mouse in which BCL2L14 is inactivated has demonstrated no apparent deleterious effects on cell types that normally express this gene (Giam et al., 2012b), perhaps suggesting some degree of functional redundancy. These authors further demonstrated that mBclG had negligible pro-apoptotic activity in human 293T cells and that the BH3 domain was incapable of binding Bcl-2 family members. Rather mBclG was capable of binding several novel partners, including transport particle protein (TRAPP) complex proteins, suggesting a potential role for mBclG in vesicle trafficking (Giam et al., 2012b). As regards pig Bcl-G, its ectopic expression in a porcine kidney cell line stimulates apoptosis induced by polyinosinic: polycytidylic acid (synthetic analogue of dsRNA and mimic of viral infection) (Jiang et al., 2012).

Homology

Homologues of BCL2L14 have been identified in a wide range of species (e.g. see Jiang et al., 2012). However, the Bcl-GS protein isoform is specific to humans (Giam et al., 2012a). Mouse and pig Bcl-G share 68% and 71% amino acid identity, respectively, with human Bcl-GL.

Implicated in

Entity name
Prostate cancer
Note
In advanced prostate cancer, deletion of 12p12 is frequently seen. Expression mapping of genes within/adjacent to the minimal deleted region in clinical tumours has demonstrated reduced expression of BCL2L14 and two other genes (DUSP16 and FLJ10298) (Kibel et al., 2004); reduced expression of BCL2L14 has been independently confirmed (Pickard et al., 2010). In the latter study, transcript levels were highly correlated with those of FAU, which also regulates apoptosis and which may act via the post-translational modification of Bcl-G (Pickard et al., 2010). Notably, down-regulation of BCL2L14 gene expression in the prostate cancer 22Rv1 cell line protects cells from apoptosis induction by ultraviolet-C irradiation (Pickard et al., 2010). BCL2L14 has been identified as a member of a four gene signature that accurately predicts prostate cancer recurrence, but high expression of BCL2L14 is associated with tumour recurrence (Latil et al., 2003).
Entity name
Breast cancer
Note
Single nucleotide polymorphisms of high frequency loss of heterozygosity that affect BCL2L14 are found more commonly in infiltrating ductal carcinoma than in infiltrating lobular carcinoma of the breast (Loo et al., 2008). In breast ductal carcinoma, BCL2L14 expression is reduced, and silencing of BCL2L14 expression in the T-47D breast cancer cell line attenuates apoptosis induction by exogenous stimuli (Pickard et al., 2009). A genome-wide RNAi screen has recently shown that BCL2L14 silencing in SKBR-3 results in resistance to the novel pan-ErbB inhibitor, neratinib (Seyhan et al., 2012). BCL2L14 has also been implicated in the anti-survival effects of nanoparticulate tetraiodothyroacetic acid on MDA-MB-231 cells (Glinskii et al., 2009).
As regards genes involved in the post-translational modification of Bcl-G, FAU expression is down-regulated and MELK expression is up-regulated in breast tumour tissue (Pickard et al., 2009). These latter changes were associated with poor patient prognosis, but no relationship was apparent between BCL2L14 gene expression and patient survival (Pickard et al., 2009), suggesting that the regulation of Bcl-G activity by post-translational modification is more important than the level of BCL2L14 expression per se in determining patient survival.
Entity name
Ovarian cancer
Note
Elevated levels of BCL2L14 gene expression have been reported for mucinous ovarian cancer relative to other histological subtypes of ovarian cancer (Heinzelmann-Schwarz et al., 2006). The functional significance of these changes are unknown. Subdivision of patients with high grade ovarian serous carcinoma into TP53 mutation-positive and p53 protein-null groups has revealed a number of differences in the genomic landscape, including gains of 12p13.2-12p13.1 (affecting DUSP16, BCL2L14 and ETV6) in the former group (Wojnarowicz et al., 2012). TP53 mutation-positive patients were also characterized by increased overall and disease-free survival (Wojnarowicz et al., 2012).
Entity name
Cervical cancer
Note
An integration site for HPV16 in cervical carcinoma has been mapped to BCL2L14 (Xu et al., 2013).
Entity name
Lung cancer
Note
Analysis of variants in inflammation pathway genes has identified single nucleotide polymorphisms of BCL2L14 in former smokers that are associated with increased risk of developing lung cancer (Spitz et al., 2012).
Entity name
Precursor B acute lymphoblastic leukemia (ALL)
Note
A novel TEL-AML1 fusion transcript, comprising an in-frame insertion of 33 nucleotides derived from BCL2L14 between exon 5 of TEL and exon 2 of AML1 has been described in a case of pediatric precursor B ALL (Abdelhaleem et al., 2006). This fusion transcript appears to be rare, and its biological effects are unknown.
Entity name
Tongue squamous cell carcinoma
Note
BCL2L14 expression has been reported to be markedly up-regulated in tongue squamous cell carcinoma tissue (Zhang et al., 2013).
Entity name
Systemic lupus erythematosus (SLE)
Note
BCL2L14 expression is up-regulated (ca. 8-fold) in CD4+ T-cells (but not CD8+ or B-cells) from patients with systemic lupus erythematosus (SLE) (Luo et al., 2009). In SLE, apoptosis is increased in CD4+ T-cells, and the degree of apoptosis in freshly isolated cells from SLE patients was directly correlated with Bcl-GL levels, as were other measures of disease activity status (Luo et al., 2009). Healthy control CD4+ T-cells in vitro demonstrated enhanced apoptosis both after transfection with a lentiviral vector expressing BclGL and after treatment with serum from SLE patients; the latter effect was associated with increased BclGL cellular levels and could be partially inhibited by prior knockdown of BclGL (Luo et al., 2009). The serum factor(s) that mediate this response remain unknown; whilst interferon-α was increased in SLE sera it alone could not account for enhanced Bcl-GL cellular levels (Luo et al., 2009).
Entity name
Innate immune response
Note
There are several reports of dysregulated expression of BCL2L14 in response to infection with a wide range of pathogens/parasites. For example, in Rhesus Macaque monkeys infected with Mycobacterium tuberculosis, BCL2L14 expression is initially enhanced in granulomas relative to normal lung tissue during the acute phase of disease but silenced several weeks post-infection (Mehra et al., 2010). While multiple markers of the pro-inflammatory response show a similar pattern, the silencing of BCL2L14 in chronic disease may contribute to pathogen survival. Studies with murine cells have further shown that exosomes derived from macrophages infected with Mycobacterium tuberculosis can block the activation of a subset of interferon-γ inducible genes, including BCL2L14, which may serve to suppress the host innate immune response beyond the site of infection (Singh et al., 2011). BCL2L14 is one of several Bcl-2 family members that is dysregulated in bovine endothelial cells following infection with the parasite Eimeria bovis (Taubert et al., 2010). It is markedly upregulated in human alveolar macrophages within a few hours of infection with H1N1 influenza A virus PR/8 (Wang et al., 2012) and it is also induced following the infection of human monocyte-derived dendritic cells with wild type Dengue 3 virus (a Flavivirus) or the chimeric CYD3 vaccine virus (Balas et al., 2011). On the other hand, BCL2L14 expression is down-regulated in porcine epithelial cells following infection with Pseudorabies virus (a herpes virus) (Flori et al., 2008).
BCL2L14 may also be implicated in the host response to viral evasion mechanisms per se. For example, selective expression of the African Swine Fever Virus evasion gene, A238L, in mouse T-lymphocytes results in the production of an aggressive lymphoma (Almeida et al., 2012). Transgenic animals exhibit massively enlarged thymuses characterized, inter alia, by enhanced BCL2L14 expression and apoptosis (Almeida et al., 2012).
While attendant changes in host cell interferon signalling may account for many of the above changes in BCL2L14 expression, it should be noted that Bcl-G can directly interact with a component of the Flavivirus replication complex (Le Breton et al., 2011). However, the biological significance of this interaction for both host and virus remains to be determined. The 3-UTR of BCL2L14 transcripts also contains potential binding sites for Epstein-Barr virus-derived miRNAs (Marquitz et al., 2011).

Article Bibliography

Pubmed IDLast YearTitleAuthors
166730182006A novel TEL-AML1 fusion transcript involving the pro-apoptotic gene BCL-G in pediatric precursor B acute lymphoblastic leukemia.Abdelhaleem M et al
225580842012Neoplastic transformation of T lymphocytes through transgenic expression of a virus host modification protein.Almeida SC et al
211485022011Different innate signatures induced in human monocyte-derived dendritic cells by wild-type dengue 3 virus, attenuated but reactogenic dengue 3 vaccine virus, or attenuated nonreactogenic dengue 1-4 vaccine virus strains.Balas C et al
170572252006A novel role for proline- and acid-rich basic region leucine zipper (PAR bZIP) proteins in the transcriptional regulation of a BH3-only proapoptotic gene.Benito A et al
212522392011Differential regulation of gene expression by protein kinase C isozymes as determined by genome-wide expression analysis.Caino MC et al
127006462003Bfk: a novel weakly proapoptotic member of the Bcl-2 protein family with a BH3 and a BH2 region.Coultas L et al
191066322008Gamma-radiation (GR) triggers a unique gene expression profile associated with cell death compared to proton radiation (PR) in mice in vivo.Finnberg N et al
183316362008Transcriptomic analysis of the dialogue between Pseudorabies virus and porcine epithelial cells during infection.Flori L et al
209783462010Loss of Nix in Pdx1-deficient mice prevents apoptotic and necrotic β cell death and diabetes.Fujimoto K et al
229640152012Arsenic trioxide and ascorbic acid interfere with the BCL2 family genes in patients with myelodysplastic syndromes: an ex-vivo study.Galimberti S et al
229143262012Detection of Bcl-2 family member Bcl-G in mouse tissues using new monoclonal antibodies.Giam M et al
230598232012Bcl-2 family member Bcl-G is not a proapoptotic protein.Giam M et al
198380612009Modification of survival pathway gene expression in human breast cancer cells by tetraiodothyroacetic acid (tetrac).Glinskii AB et al
110544132001Bcl-G, a novel pro-apoptotic member of the Bcl-2 family.Guo B et al
165086392006A distinct molecular profile associated with mucinous epithelial ovarian cancer.Heinzelmann-Schwarz VA et al
229805162012BCL-G as a new candidate gene for immune responses in pigs: bioinformatic analysis and functional characterization.Jiang P et al
149997722004Expression mapping at 12p12-13 in advanced prostate carcinoma.Kibel AS et al
146545262003Gene expression profiling in clinically localized prostate cancer: a four-gene expression model predicts clinical behavior.Latil A et al
220141112011Flavivirus NS3 and NS5 proteins interaction network: a high-throughput yeast two-hybrid screen.Le Breton M et al
172806162007Involvement of maternal embryonic leucine zipper kinase (MELK) in mammary carcinogenesis through interaction with Bcl-G, a pro-apoptotic member of the Bcl-2 family.Lin ML et al
180062762008JAB1 accelerates mitochondrial apoptosis by interaction with proapoptotic BclGs.Liu X et al
187205242008Differential patterns of allelic loss in estrogen receptor-positive infiltrating lobular and ductal breast cancer.Loo LW et al
195244892009Upregulated BclG(L) expression enhances apoptosis of peripheral blood CD4+ T lymphocytes in patients with systemic lupus erythematosus.Luo N et al
213333172011The Epstein-Barr Virus BART microRNAs target the pro-apoptotic protein Bim.Marquitz AR et al
208242052010Transcriptional reprogramming in nonhuman primate (rhesus macaque) tuberculosis granulomas.Mehra S et al
159585532005A genomic map of p53 binding sites identifies novel p53 targets involved in an apoptotic network.Miled C et al
152848602004Mutational and expression analysis of the chromosome 12p candidate tumor suppressor genes in pre-B acute lymphoblastic leukemia.Montpetit A et al
166217902006The ubiquitin-like protein MNSFbeta regulates ERK-MAPK cascade.Nakamura M et al
184652082008Comparison of the effects of 40% oxygen and two atmospheric absolute air pressure conditions on stress-induced premature senescence of normal human diploid fibroblasts.Oh S et al
215503982011Candidate tumour suppressor Fau regulates apoptosis in human cells: an essential role for Bcl-G.Pickard MR et al
224469322012A genome-wide RNAi screen identifies novel targets of neratinib resistance leading to identification of potential drug resistant genetic markers.Seyhan AA et al
215331722011Exosomes released from M. tuberculosis infected cells can suppress IFN-γ mediated activation of naïve macrophages.Singh PP et al
164840052006BH3 domain mutation of proapoptotic genes Bad, Bmf and Bcl-G is rare in transitional cell carcinomas of the urinary bladder.Soung YH et al
225737962012Multistage analysis of variants in the inflammation pathway and lung cancer risk in smokers.Spitz MR et al
206153802010Microarray-based transcriptional profiling of Eimeria bovis-infected bovine endothelial host cells.Taubert A et al
194404502008MicroRNA and Cancer: Tiny Molecules with Major Implications.Vandenboom Ii TG et al
223967272012Innate immune response of human alveolar macrophages during influenza A infection.Wang J et al
232981872013Ubiquitin-like protein MNSFβ covalently binds to Bcl-G and enhances lipopolysaccharide/interferon γ-induced apoptosis in macrophages.Watanabe J et al
230290432012The genomic landscape of TP53 and p53 annotated high grade ovarian serous carcinomas from a defined founder population associated with patient outcome.Wojnarowicz PM et al
238246732013Multiplex Identification of Human Papillomavirus 16 DNA Integration Sites in Cervical Carcinomas.Xu B et al
175575682007Mutational analysis of the BH3 domains of proapoptotic Bcl-2 family genes Bad, Bmf and Bcl-G in laryngeal squamous cell carcinomas.Yoo NJ et al
234467312013Genome-wide analysis of DNA methylation in tongue squamous cell carcinoma.Zhang S et al
169875582006Hyper-activated IRF-1 and STAT1 contribute to enhanced interferon stimulated gene (ISG) expression by interferon alpha and gamma co-treatment in human hepatoma cells.Zhang XN et al

Other Information

Locus ID:

NCBI: 79370
MIM: 606126
HGNC: 16657
Ensembl: ENSG00000121380

Variants:

dbSNP: 79370
ClinVar: 79370
TCGA: ENSG00000121380
COSMIC: BCL2L14

RNA/Proteins

Gene IDTranscript IDUniprot
ENSG00000121380ENST00000266434Q9BZR8
ENSG00000121380ENST00000266434A0A140VJF2
ENSG00000121380ENST00000298566Q9BZR8
ENSG00000121380ENST00000308721Q9BZR8
ENSG00000121380ENST00000308721A0A024RAR1
ENSG00000121380ENST00000396367Q9BZR8
ENSG00000121380ENST00000396367A0A024RAR1
ENSG00000121380ENST00000461264C9K0Q9
ENSG00000121380ENST00000464885C9J3S1
ENSG00000121380ENST00000586576K7EMX4
ENSG00000121380ENST00000588270K7EKK7
ENSG00000121380ENST00000589718Q9BZR8
ENSG00000121380ENST00000589718A0A024RAR1

Expression (GTEx)

0
5
10
15
20
25
30

Pathways

PathwaySourceExternal ID
Gene ExpressionREACTOMER-HSA-74160
Generic Transcription PathwayREACTOMER-HSA-212436
Transcriptional Regulation by TP53REACTOMER-HSA-3700989
TP53 Regulates Transcription of Cell Death GenesREACTOMER-HSA-5633008
TP53 regulates transcription of several additional cell death genes whose specific roles in p53-dependent apoptosis remain uncertainREACTOMER-HSA-6803205

Protein levels (Protein atlas)

Not detected
Low
Medium
High

References

Pubmed IDYearTitleCitations
312969632020Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer.6
319882962020Human BCL-G regulates secretion of inflammatory chemokines but is dispensable for induction of apoptosis by IFN-γ and TNF-α in intestinal epithelial cells.16
323218292020Landscape analysis of adjacent gene rearrangements reveals BCL2L14-ETV6 gene fusions in more aggressive triple-negative breast cancer.13
312969632020Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer.6
319882962020Human BCL-G regulates secretion of inflammatory chemokines but is dispensable for induction of apoptosis by IFN-γ and TNF-α in intestinal epithelial cells.16
323218292020Landscape analysis of adjacent gene rearrangements reveals BCL2L14-ETV6 gene fusions in more aggressive triple-negative breast cancer.13
305972312019Upregulation of miR-496 decreases cerebral ischemia/reperfusion injury by negatively regulating BCL2L14.14
305972312019Upregulation of miR-496 decreases cerebral ischemia/reperfusion injury by negatively regulating BCL2L14.14
300751512018Medullary Breast Carcinoma, a Triple-Negative Breast Cancer Associated with BCLG Overexpression.10
300751512018Medullary Breast Carcinoma, a Triple-Negative Breast Cancer Associated with BCLG Overexpression.10
230770882013Abnormalities of the der(12)t(12;21) in ETV6-RUNX1 acute lymphoblastic leukemia.5
230770882013Abnormalities of the der(12)t(12;21) in ETV6-RUNX1 acute lymphoblastic leukemia.5
225737962012Multistage analysis of variants in the inflammation pathway and lung cancer risk in smokers.20
225737962012Multistage analysis of variants in the inflammation pathway and lung cancer risk in smokers.20
215503982011Candidate tumour suppressor Fau regulates apoptosis in human cells: an essential role for Bcl-G.17

Citation

Mark R Pickard ; Gwyn T Williams

BCL2L14 (BCL2-like 14 (apoptosis facilitator))

Atlas Genet Cytogenet Oncol Haematol. 2013-08-01

Online version: http://atlasgeneticsoncology.org/gene/774/tumors-explorer/deep-insight-explorer/