Human Bcl-w / BCL2L2 Protein
- Known as:
- Human Bcl-w / BCL2L2 Protein
- Catalog number:
- BC2-H5122
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human Bcl- / BCL2L2 Protein
Ask about this productRelated genes to: Human Bcl-w / BCL2L2 Protein
- Gene:
- BCL2 NIH gene
- Name:
- BCL2 apoptosis regulator
- Previous symbol:
- -
- Synonyms:
- Bcl-2, PPP1R50
- Chromosome:
- 18q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
- Gene:
- BCL2L1 NIH gene
- Name:
- BCL2 like 1
- Previous symbol:
- -
- Synonyms:
- BCLX, BCL2L, Bcl-X, bcl-xL, bcl-xS, PPP1R52
- Chromosome:
- 20q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-30
- Date modifiied:
- 2016-01-13
- Gene:
- BCL2L2 NIH gene
- Name:
- BCL2 like 2
- Previous symbol:
- -
- Synonyms:
- KIAA0271, BCL-W, PPP1R51
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-22
- Date modifiied:
- 2016-10-05
- Gene:
- BCL9L NIH gene
- Name:
- BCL9 like
- Previous symbol:
- -
- Synonyms:
- DLNB11, B9L, Bcl9-2
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-09
- Date modifiied:
- 2018-11-16
Related products to: Human Bcl-w / BCL2L2 Protein
Related articles to: Human Bcl-w / BCL2L2 Protein
- L. () is a shrub that has been widely used in European folk medicine as an anti-inflammatory and antimicrobial agent. The purpose of our study was to elucidate the mechanisms of the chemopreventive action of the plant's methanolic root extract (BVR) against colon cancer cells. Studies were conducted in human colon adenocarcinoma cell lines (LS180 and HT-29) and control colon epithelial CCD841 CoN cells. According to the MTT assay, after 48 h of cell exposure, the IC values were as follows: 4.3, 46.1, and 50.2 µg/mL for the LS180, HT-29, and CCD841 CoN cells, respectively, showing the greater sensitivity of the cancer cells to BVR. The Cell Death Detection ELISAPLUS kit demonstrated that BVR induced programmed cell death only against HT-29 cells. Nuclear double staining revealed the great proapoptotic BVR properties in HT-29 cells and subtle effect in LS180 cells. RT-qPCR with the relative quantification method showed significant changes in the expression of genes related to apoptosis in both the LS180 and HT-29 cells. The genes (126.86-421.43%), (240-286.02%), (177.19-247.83%), and (157.99-243.75%) had a significantly elevated expression, while BCL2 (25-52.03%) had a reduced expression compared to the untreated control. Furthermore, in a panel of antioxidant tests, BVR showed positive effects (63.93 ± 0.01, 122.92 ± 0.01, and 220.29 ± 0.02 mg Trolox equivalents (TE)/g in the DPPH•, ABTS•+, and ORAC assays, respectively). In the lipoxygenase (LOX) inhibition test, BVR revealed 62.60 ± 0.87% of enzyme inhibition. The chemical composition of BVR was determined using a UHPLC-UV-CAD-MS/MS analysis and confirmed the presence of several known alkaloids, including berberine, as well as other alkaloids and two derivatives of hydroxycinnamic acid (ferulic and sinapic acid hexosides). The results are very promising and encourage the use of BVR as a comprehensive chemopreventive agent (anti-inflammatory, antioxidant, and pro-apoptotic) in colorectal cancer, and were widely discussed alongside data from the literature. - Source: PubMed
Publication date: 2024/04/27
Och AnnaLemieszek Marta KingaCieśla MarekJedrejek DariuszKozłowska AleksandraPawelec SylwiaNowak Renata - Circumvention of apoptosis by the elevation of antiapoptotic proteins is an important cause of carcinogenesis. The induction of antiapoptotic genes, including B-cell CLL/lymphoma 2 (BCL2), BCL2 related protein A1 (BCL2A1), BCL2 like 1 (BCL2L1), BCL2L2, and myeloid cell leukemia 1 (MCL1), has been observed in multiple cancers, including breast cancer. However, the underlying mechanisms of their overexpression are still being investigated. Here, we revealed that BCL2, BCL2A1, BCL2L2, and MCL1 but not BCL2L1 were overexpressed in estrogen receptor (ER)-positive breast cancer cells and clinical biopsies. Stimulation with estrogen in ER-positive cell lines resulted in a dose-dependent increase in BCL2, BCL2A1, BCL2L2, and MCL1 mRNA levels. Molecular investigation revealed that nuclear factor kappa B (NF-κB) recruited histone acetyltransferase p300 and nuclear receptor coactivator 3 (NCOA3) to form a transcriptional complex. This complex docked the promoters of BCL2, BCL2A1, BCL2L2, and MCL1 and activated their expression. Interestingly, estrogen exposure dose-dependently activated NCOA3. Depletion of the NCOA3-p300-NF-κB components or blockage of NCOA3 function with inhibitors (gossypol and bufalin) in ER-positive cells suppressed BCL2, BCL2A1, BCL2L2, and MCL1 expression, while also decreasing cell viability, colony formation, cell invasion, and tumor growth. Collectively, our results demonstrate an upstream signaling that activates four antiapoptotic genes in ER-positive breast cancer cells. Importantly, our results also imply that targeting NCOA3 or blocking the assembly of the NCOA3-p300-NF-κB complex may be promising therapeutic strategies for treating ER-positive breast cancer. - Source: PubMed
Publication date: 2023/02/28
Wang JunZhou Zhiyong - Tumor cells proliferation and apoptosis inhibition are the mechanisms through which the Colorectal Cancer (CRC) progression, metastasis and chemoresistance are promoted pathologically, offering clinical advantages for characterizing their molecular regulators. - Source: PubMed
Publication date: 2023/01/01
Kishani Farahani RoyaSoleimanpour SamerehGolmohammadi MaryamSoleimanpour-Lichaei Hamid Reza - Progress in therapies and improved outcomes in recent decades have followed a better understanding of breast cancers pathogenesis and their heterogeneity but new treatments are needed especially for metastatic disease which remains incurable. Inhibition of apoptosis is a hallmark characteristic of cancer and can be targeted for therapy. - Source: PubMed
Publication date: 2023/01/07
Voutsadakis Ioannis A - Breast cancer is one of the most prevalent cancers and a cause of significant morbidity and mortality. Despite introduction of new therapies that improve control of the disease, metastatic breast cancer remains still incurable in most cases. Further therapies based on a better understanding of the pathogenesis of breast cancers and its sub-types are needed to improve outcomes. Apoptosis has arisen as a potential target in recent years. Research on therapeutic use of apoptosis promoting drugs could be advanced by cell line models of efficacy. - Source: PubMed
Publication date: 2022/09/11
Voutsadakis Ioannis A