| 1999 |
BCAS2 (DAM1) was identified as a novel gene amplified at chromosome 1p13.3-21 in human breast cancer cell lines MCF-7 and BT-20, encoding a 26-kDa protein upregulated by gene amplification. |
RNA differential display, Southern blot analysis, chromosomal mapping |
Cancer letters |
Medium |
10403562
|
| 2002 |
BCAS2 protein localizes to the nucleus, as shown by enhanced green fluorescent protein (EGFP) fusion assay in breast cancer cells. |
EGFP fusion protein localization assay |
Cancer letters |
Medium |
12169396
|
| 2002 |
Mouse BCAS2 (mDAM1) interacts with the Src-family kinase BLK in vitro and in vivo, and co-expression of mDAM1 with BLK increases cell death compared to BLK alone in NMuMG mammary epithelial cells, indicating BCAS2 promotes pro-apoptotic activity of BLK. |
Yeast two-hybrid screen, in vitro protein binding assay, stable transfection with cell death assay |
Cancer letters |
Medium |
12406557
|
| 2012 |
Drosophila BCAS2 (dBCAS2) is essential for viability and functions in pre-mRNA splicing; its depletion causes impaired splicing and apoptosis. The C-terminal coiled-coil domain of human BCAS2 directly binds CDC5L and recruits hPrp19/PLRG1 to form a core splicing complex. Overexpression of hBCAS2 rescues Drosophila dBCAS2 depletion phenotypes, demonstrating functional conservation. |
RNAi knockdown in Drosophila, rescue with human BCAS2, direct binding assay (C-terminal coiled-coil domain), co-immunoprecipitation |
RNA (New York, N.Y.) |
High |
23249746
|
| 2014 |
BCAS2 is a direct transcriptional target of ERRβ and mediates ERRβ-dependent inhibition of FST transcription through downregulation of β-catenin/TCF4 recruitment to the FST promoter. ERRβ-mediated upregulation of BCAS2 downregulates cyclin D1, blocking G1/S transition in breast cancer cells. |
ChIP cloning, gel supershift assays, co-immunoprecipitation, confocal microscopy, western blotting, quantitative RT-PCR, luciferase assay |
British journal of cancer |
Medium |
24667650
|
| 2014 |
BCAS2 interacts directly with androgen receptor (AR) and HSP90, stabilizing AR protein from proteasomal degradation via two mechanisms: (1) p53-dependent suppression increasing AR mRNA and protein, and (2) p53-independent inhibition of proteasome degradation through BCAS2-AR-HSP90 complex formation. |
GST pull-down assay, co-immunoprecipitation, luciferase assay, MTT assay, western blotting, immunohistochemistry |
British journal of cancer |
High |
25461807
|
| 2014 |
In Ustilago maydis, the SPF27/BCAS2 homologue Num1 functions as a core NTC/PRP19 complex component required for pre-mRNA splicing (global intron retention upon deletion) and additionally interacts with the kinesin motor Kin1 in the cytoplasm, connecting splicing to cytoplasmic vesicle trafficking and polarized growth. |
RNA-seq (intron retention), yeast two-hybrid/interactome screen, co-immunoprecipitation, genetic phenotypic analysis |
PLoS genetics |
Medium |
24391515
|
| 2015 |
Maternal BCAS2 maintains genome integrity in mouse early embryos by functioning through the RPA complex: BCAS2 responds to DNA damage in zygotes, and BCAS2 mutants unable to bind RPA1 fail to support DNA repair. Phosphorylated RPA2 cannot localize to DNA damage sites when maternal BCAS2 is disrupted, establishing BCAS2's role in the DNA damage response via RPA. |
Maternal depletion (morpholino/siRNA injection in zygotes), immunofluorescence, DNA damage assays, mutant rescue experiments, co-immunoprecipitation |
Development (Cambridge, England) |
High |
26428007
|
| 2015 |
BCAS2 negatively regulates HSF4 protein stability by promoting its ubiquitination at lysine 206; knockdown of BCAS2 increases HSF4 protein half-life and reduces ubiquitination. The HSF4-K206R mutant blocks BCAS2's impact on HSF4 stability, implicating BCAS2 in HSF4 degradation via the ubiquitin-proteasome system. |
Co-immunoprecipitation, western blotting, cycloheximide chase (protein half-life), site-directed mutagenesis (K206R), ubiquitination assay |
The international journal of biochemistry & cell biology |
High |
26319152
|
| 2015 |
BCAS2 regulates Delta-Notch signaling in Drosophila wing development through pre-mRNA splicing of Delta; dBCAS2 depletion reduces Delta mRNA, causes accumulation of Delta pre-mRNA, and diminishes transcription of Notch target genes (cut, E(spl)m8). Overexpression of Delta rescues dBCAS2 depletion wing deformation, and ectopic expression of hBCAS2 or dBCAS2 rescues pre-mRNA splicing defects. |
RNAi knockdown, RT-PCR (pre-mRNA accumulation), genetic rescue experiments, reporter gene assays |
PloS one |
High |
26091239
|
| 2016 |
Conditional knockout of BCAS2 in mouse forebrain causes dendritic malformation; exon array analysis identified β-catenin pre-mRNA as a splicing target of BCAS2. Overexpression of β-catenin in BCAS2-depleted primary neurons restores dendritic growth, placing BCAS2 upstream of β-catenin in a pathway regulating dendrite development. |
Conditional knockout mouse model, exon array assay, Golgi staining, BrdU incorporation, DCX immunostaining, β-catenin overexpression rescue |
Scientific reports |
High |
27713508
|
| 2017 |
BCAS2 is specifically enriched in spermatogonia and is required for alternative splicing in male germ cells and the transition to meiosis. Conditional disruption of Bcas2 in male germ cells alters alternative splicing of 245 genes including Dazl, Ehmt2, and Hmga1; loss of BCAS2 causes decrease in full-length DAZL protein and increase of a short form lacking exon 8, impairing meiosis initiation. |
Conditional knockout mouse model, alternative splicing analysis (RNA-seq), western blotting, immunofluorescence, histological analysis of spermatogenesis |
Nature communications |
High |
28128212
|
| 2017 |
miR-486 targets BCAS2 (and CDK4) in esophageal cancer cells; dual-luciferase reporter assay confirmed BCAS2 as a direct target of miR-486. Knockdown of BCAS2 phenocopies miR-486 overexpression, inducing G0/G1 arrest and apoptosis, with upregulation of p21 and caspase-3. |
Dual-luciferase reporter gene assay, siRNA knockdown, flow cytometry, western blotting |
Oncology reports |
Medium |
29115564
|
| 2018 |
BCAS2 is essential for hematopoietic stem and progenitor cell (HSPC) maintenance in zebrafish; bcas2 knockout induces abnormal alternative splicing of Mdm4 (producing a pro-apoptotic isoform), leading to p53-mediated HSPC apoptosis. Suppression of p53 rescues the HSPC deficiency, establishing a BCAS2 → Mdm4 splicing → p53 pathway. |
TALEN-mediated knockout in zebrafish, alternative splicing analysis, p53 suppression rescue experiments, TUNEL assay, in situ hybridization |
Blood |
High |
30482793
|
| 2018 |
In Ustilago maydis, the SPF27/BCAS2 homologue Num1 localizes predominantly in the nucleus but also in the cytoplasm near microtubules; its cytoplasmic movement depends on interaction with kinesin Kin1 (not Kin3), as shown by super-resolution localization microscopy. |
Super-resolution localization microscopy (STORM/PALM with tdEosFP fusion), particle tracking analysis, genetic dependency on Kin1 vs Kin3 |
Scientific reports |
Medium |
29483520
|
| 2019 |
BCAS2 interacts with ERα both in vitro and in vivo and upregulates ERα transcriptional activity through the AF-1 (N-terminal) region of ERα directly, and indirectly through the AF-2 (C-terminal) region by acting in concert with AF-2 coactivators. BCAS2 is regulated preferentially by the PI3K/AKT signaling pathway in breast cancer cells. |
Co-immunoprecipitation, GST pull-down (protein-protein interaction), luciferase reporter assay, signal transduction inhibitor experiments |
International journal of molecular sciences |
Medium |
30813351
|
| 2020 |
BCAS2 enhances both non-homologous end joining (NHEJ) and homologous recombination (HR) DNA double-strand break repair pathways by directly interacting with NBS1; this interaction involves the BCAS2 N-terminus and both the NBS1 N- and C-termini, as defined by GST pull-down and co-immunoprecipitation assays. |
GST pull-down assay, co-immunoprecipitation, precise end-joining assay (NHEJ), flow cytometry (HR), immunofluorescence, radiation-induced DSB repair assay |
British journal of cancer |
High |
32963349
|
| 2022 |
BCAS2 (as an RNA binding protein) regulates the expression of circular RNA circ_002363 by interacting with Pre-DNA2, the host gene of circ_002363, in bronchial epithelial cells exposed to neodymium oxide nanoparticles, as shown by RNA pull-down and western blot assays. |
RNA pull-down assay, western blot, RT-qPCR, functional DNA damage assays |
The Science of the total environment |
Low |
36526188
|
| 2023 |
BCAS2 regulates oocyte meiotic prophase I by participating in alternative splicing through the PRP19 complex (with CDC5L and PRP19); conditional knockout of Bcas2 in oocytes during pachytene phase causes infertility, primordial follicle depletion, and abnormal alternative splicing of Dazl and Diaph2. |
Conditional knockout mouse model (Stra8-GFPCre), RNA-seq alternative splicing analysis, immunostaining, fertility testing |
FASEB journal |
High |
38085152
|
| 2023 |
BCAS2 regulates granulosa cell survival by participating in alternative splicing of E2f3 and Flt3l mRNA through the PRP19 complex (with CDC5L and PRP19); Bcas2 knockout in granulosa cells causes cell cycle arrest, DNA damage, apoptosis, and abnormal RPA1 staining. |
Conditional knockout mouse model, RNA-seq, BrdU incorporation assay, immunostaining, co-immunoprecipitation (PRP19 complex) |
Journal of ovarian research |
High |
37248466
|
| 2023 |
BCAS2 participates in insulin synthesis and secretion in pancreatic β-cells via alternative splicing; Bcas2 conditional knockout in β-cells causes glucose intolerance and decreased insulin secretion granules, linked to abnormal splicing of Syt7 and Tcf7l2 pre-mRNA. |
Conditional knockout mouse model (Bcas2 f/f-βKO), glucose tolerance test, insulin secretion assay, immunohistochemistry, electron microscopy of secretion granules, alternative splicing analysis |
Endocrinology |
High |
37820033
|
| 2024 |
BCAS2 directly binds 5' splice sites (5'SS) of introns and GA-rich regions in testis (mapped by CLIP-seq); it regulates alternative splicing of Trp53bp1 (53BP1) and Six6os1 during meiotic prophase I DSB repair and synapsis. BCAS2 interacts with hnRNPH1 and SRSF3 to orchestrate Trp53bp1 expression via alternative splicing. |
CLIP-seq (crosslinking immunoprecipitation and sequencing), conditional knockout mouse model, co-immunoprecipitation, RNA-seq |
Cellular and molecular life sciences |
High |
39520542
|
| 2025 |
BCAS2 promotes primitive hematopoiesis by directly binding to β-catenin via its coiled-coil domains and sequestering β-catenin within the nucleus, thereby enhancing Wnt/β-catenin signaling. BCAS2 deficiency reduces β-catenin nuclear accumulation without affecting β-catenin pre-mRNA splicing, revealing a splicing-independent nuclear retention function. |
bcas2 knockout in zebrafish and mouse embryonic fibroblasts, co-immunoprecipitation, domain mapping (coiled-coil), β-catenin localization assay, Wnt reporter assay, splicing analysis |
eLife |
High |
40511787
|
| 2025 |
BCAS2 regulates antibody class switch recombination (CSR) in activated B cells by interacting with SRSF7 at a conserved circular domain to form a complex that controls alternative splicing of genes involved in post-switch transcription. BCAS2 binds RNA at GAAGAA motifs (identified by CLIP-seq). A mutation at the 3'UTR of Bcas2 was found in children with hyper-IgM syndrome type 1, with similar AS and CSR patterns. |
Conditional knockout mouse model (AID-Cre Bcas2 fl/fl), CLIP-seq, RNA-sequencing, co-immunoprecipitation, interactome proteomics |
Exploration (Beijing, China) |
High |
40585763
|
| 2026 |
BCAS2 interacts with hnRNPM and modulates its binding to pre-mRNA loci to control alternative splicing during oocyte development; LACE-seq revealed hnRNPM-binding sites at single-nucleotide resolution and showed that hnRNPM-BCAS2 interaction is required for splicing fidelity in growing oocytes. |
Genetic ablation of hnRNPM, LACE-seq (RNA-binding site mapping), SCAN-seq (single-cell), co-immunoprecipitation |
Nature communications |
Medium |
41680151
|