Lower Chamber, AE _6450
- Known as:
- Lower Chamber, AE _6450
- Catalog number:
- 2398250
- Category:
- -
- Supplier:
- Ato
- Gene target:
- Lower Chamber _6450
Related genes to: Lower Chamber, AE _6450
- Gene:
- BICDL1 NIH gene
- Name:
- BICD family like cargo adaptor 1
- Previous symbol:
- CCDC64
- Synonyms:
- FLJ26450, BICDR-1
- Chromosome:
- 12q24.23
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-24
- Date modifiied:
- 2016-05-03
Related products to: Lower Chamber, AE _6450
Related articles to: Lower Chamber, AE _6450
- Elevated levels of Bicaudal-D Family Like Cargo Adaptor 1 (BICDL1) are associated with poor prognosis in various cancers. However, the role of BICDL1 in breast cancer (BC) has not been reported. We analyzed BICDL1 expression in BC using bioinformatics and molecular experiments. Gene Set Enrichment Analysis was conducted to identify significantly enriched signaling pathways related to BICDL1. The effects of BICDL1 on BC cell proliferation, migration, invasion, and expression of epithelial-mesenchymal transition (EMT)-related proteins were assessed using colony formation assays, Transwell assays, and Western blot. The influence of BICDL1 on pyroptosis in BC cells was determined by measuring the expression of key pyroptosis proteins (NLRP3, GSDMD-N, procaspase-1, cleaved caspase-1, ASC), lactate dehydrogenase release, and cytokines (IL-1β and IL-18). We also investigated whether BICDL1 promotes BC proliferation and metastasis by regulating pyroptosis using Nigericin, an agent that induces NLRP3 inflammasome activation. The results showed that BICDL1 was significantly overexpressed in BC tissues and cells. Knockdown of BICDL1 inhibited BC cell proliferation, migration, invasion, and the EMT process, while overexpression of BICDL1 had the opposite effects. BICDL1 was enriched in the pyroptosis pathway; overexpression of BICDL1 suppressed pyroptosis, thus promoting BC cell proliferation, inhibition, and migration. Notably, the addition of Nigericin reversed the effects of BICDL1 overexpression on BC cells. These results suggested that BICDL1 promoted BC cell proliferation, inhibition, and migration by hindering pyroptosis. These findings indicate that BICDL1 is a potential biomarker for BC treatment. - Source: PubMed
Publication date: 2025/09/15
Chu XuXiang LingZou YanLi XiangZhang NaZhao Hao - Bicaudal-D (BICD) Family Like Cargo Adaptor 1 (BICDL1) is an essential component of the molecular mechanism during neuronal development. However, BICDL1 has not been reported in cancer. Using bioinformatics analysis, we systematically evaluated the potential role of BICDL1 in CRC. - Source: PubMed
Publication date: 2023/12/22
Luo HongbiaoLuo JiDing NingZhang TaoHe Yongheng - Dynein and its cofactor dynactin form a highly processive microtubule motor in the presence of an activating adaptor, such as BICD2. Different adaptors link dynein and dynactin to distinct cargoes. Here we use electron microscopy and single-molecule studies to show that adaptors can recruit a second dynein to dynactin. Whereas BICD2 is biased towards recruiting a single dynein, the adaptors BICDR1 and HOOK3 predominantly recruit two dyneins. We find that the shift towards a double dynein complex increases both the force and speed of the microtubule motor. Our 3.5 Å resolution cryo-electron microscopy reconstruction of a dynein tail-dynactin-BICDR1 complex reveals how dynactin can act as a scaffold to coordinate two dyneins side-by-side. Our work provides a structural basis for understanding how diverse adaptors recruit different numbers of dyneins and regulate the motile properties of the dynein-dynactin transport machine. - Source: PubMed
Urnavicius LinasLau Clinton KElshenawy Mohamed MMorales-Rios EdgarMotz CarinaYildiz AhmetCarter Andrew P - Membrane and secretory trafficking are essential for proper neuronal development. However, the molecular mechanisms that organize secretory trafficking are poorly understood. Here, we identify Bicaudal-D-related protein 1 (BICDR-1) as an effector of the small GTPase Rab6 and key component of the molecular machinery that controls secretory vesicle transport in developing neurons. BICDR-1 interacts with kinesin motor Kif1C, the dynein/dynactin retrograde motor complex, regulates the pericentrosomal localization of Rab6-positive secretory vesicles and is required for neural development in zebrafish. BICDR-1 expression is high during early neuronal development and strongly declines during neurite outgrowth. In young neurons, BICDR-1 accumulates Rab6 secretory vesicles around the centrosome, restricts anterograde secretory transport and inhibits neuritogenesis. Later during development, BICDR-1 expression is strongly reduced, which permits anterograde secretory transport required for neurite outgrowth. These results indicate an important role for BICDR-1 as temporal regulator of secretory trafficking during the early phase of neuronal differentiation. - Source: PubMed
Publication date: 2010/04/01
Schlager Max AKapitein Lukas CGrigoriev IlyaBurzynski Grzegorz MWulf Phebe SKeijzer Nandade Graaff EstherFukuda MitsunoriShepherd Iain TAkhmanova AnnaHoogenraad Casper C