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Validated All-in-One™ qPCR Primer for BECN1(NM_001313998.2) Search again
Product ID:
HQP164474
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ATG6, VPS30, beclin1
Gene Description:
beclin 1
Target Gene Accession:
NM_001313998.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Gene References into function
- expression of three (Beclin 1, RbAp48 and Pir51) were increased and one (aldolase b) was decreased in liver tumor tissues.
- C(2)-ceramide stimulated macroautophagy in colon cancer cells, stimulated the expression of the autophagy gene product beclin 1, and mediated tamoxifen-dependent accumulation of autophagic vacuoles in breast cancer MCF-7 cells
- BECLIN 1 augmented cisplatin-induced apoptosis via enhancing caspase 9 activity.
- VPS30/ATG6 complemented A1PiZ degradation-deficient (add3) yeast mutants
- Results argue against a role for Beclin 1 as an essential chaperone or adaptor for hVps34 in normal vesicular trafficking, and they support the hypothesis that Beclin 1 functions mainly to engage hVps34 in the autophagic pathway.
- age-dependent decrease of beclin 1 expression may lead to a reduction of autophagic activity during aging, which in turn promotes the accumulation of mutant Htt and the progression of the disease
- Partial Beclin 1 silencing aggravates mitochondrial permeabilization and apoptosis in HepG2 cells treated with an anti-Fas antibody or with doxorubicin
- Evolutionarily conserved domain of Beclin 1 is essential for Vps34 interaction, autophagy function, and tumor suppressor function.
- Beclin 1 has different roles in different histotypes of human brain tumours
- Kringle 5 of human plasminogen has a role in autophagic survival by up-regulating Beclin 1 and complexing Bcl-2 to Beclin 1
- BH3-only proteins and BH3 mimetics induce autophagy by competitively disrupting the interaction between BECN1 and Bcl-2/Bcl-X(L).
- The functional and physical interaction between Bcl-X(L) and a BH3-like domain in BECN1 was studied.
- this is the first report on BECN1 gene mutations in human cancer tissues, and the data suggest that point mutations are a rare event in common human cancers and probably do not play a major role in cancer pathogenesis
- These results indicate that Beclin 1 can inhibit the growth of colorectal cancer cells.
- Differential interactions between BECN1 and Bcl-2 family members are reported.
- Analysis of all known Bcl-xL/BH3 domain complexes.
- Autophagy also plays an essential role in tumorigenesis, as the essential autophagy regulator BECN1 is monoallelically deleted.
- Data suggest that beclin 1 plays important roles in the regulation of the life span of human CL and ovarian androgen-secreting cells, by maintaining autophagy at levels promoting cell survival rather than cell death.
- Data suggest that ICP34.5-mediated antagonism of the autophagy function of Beclin 1 is essential for viral neurovirulence, and the antiviral signaling molecule PKR lies genetically upstream of Beclin 1 in host defense against HSV-1.
- beclin-1 inactivation by loss of expression may not occur in colorectal and gastric cancers
- Abeta pathology is regulated by beclin 1 through a pathway that involves autophagy
- beclin 1 deficiency disrupts neuronal autophagy, modulates APP metabolism, and promotes neurodegeneration
- Data suggest that a Beclin1-binding autophagic tumour suppressor, UVRAG, interacts with the class C Vps complex, a key component of the endosomal fusion machinery.
- beclin 1 has a role in vitamin D3-induced autophagy of human myeloid leukemia cells
- Bcl-xL and UVRAG cause a monomer-dimer switch in Beclin1
- These results demonstrate that Beclin 1 is essential for autophagy, differentiation and antiapoptosis, and may play an important role in coordinating inputs for cellular decisions to signaling machinery that mediates different cellular cascades.
- gamma-Herpesvirus protein M11 inhibits autophagy through a mechanism that involves the binding of the Beclin 1 BH3 domain in the M11 hydrophobic surface groove.
- Beclin 1 can down-regulate estrogenic signaling and growth response, and contribute to the development of antiestrogen resistance.
- These results suggest that mammalian cells have at least two distinct class III PI3-kinase complexes, and that beclin 1 interacts distinctly with mammalian Atg14 and UVRAG in two of these complexes.
- study defines a regulatory signaling pathway mediated by Barkor (KIAA0831) that positively controls autophagy through Beclin 1