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  4. Recombinant Human Bcl-2 homologous antagonist/killer (BAK1)

Recombinant Human Bcl-2 homologous antagonist/killer (BAK1)

  • 货号：
    CSB-CF624111HU
  • 规格：
  • 来源：
    in vitro E.coli expression system
  • 其他：

产品详情

  • 基因名：
  • Uniprot No.：
  • 别名：
    BAK1; BAK; BCL2L7; CDN1; Bcl-2 homologous antagonist/killer; Apoptosis regulator BAK; Bcl-2-like protein 7; Bcl2-L-7
  • 种属：
    Homo sapiens (Human)
  • 蛋白长度：
    full length protein
  • 表达区域：
    1-211
  • 氨基酸序列
    MASGQGPGPPRQECGEPALPSASEEQVAQDTEEVFRSYVFYRHQQEQEAEGVAAPADPEM VTLPLQPSSTMGQVGRQLAIIGDDINRRYDSEFQTMLQHLQPTAENAYEYFTKIATSLFE SGINWGRVVALLGFGYRLALHVYQHGLTGFLGQVTRFVVDFMLHHCIARWIAQRGGWVAA LNLGNGPILNVLVVLGVVLLGQFVVRRFFKS
    Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
  • 蛋白标签：
    N-terminal 10xHis-tagged
  • 产品提供形式：
    Liquid or Lyophilized powder
    Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
  • 缓冲液：
    Lyophilized from Tris/PBS-based buffer, 6% Trehalose, pH 8.0
  • 储存条件：
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保质期：
    The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
    Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
  • 货期：
    Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
    Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
  • 注意事项：
    Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
  • Datasheet & COA：
    Please contact us to get it.

产品评价

靶点详情

  • 功能：
    Plays a role in the mitochondrial apoptosic process. Upon arrival of cell death signals, promotes mitochondrial outer membrane (MOM) permeabilization by oligomerizing to form pores within the MOM. This releases apoptogenic factors into the cytosol, including cytochrome c, promoting the activation of caspase 9 which in turn processes and activates the effector caspases.
  • 基因功能参考文献：
    1. Our findings suggested that ZBP-89 and Sp1 overexpression induced Bak expression in a genetic manner. Increased Bak level was associated with poor patient survival, whereas high level of Sp1 is a beneficial factor for patient survival. PMID: 29653560
    2. Study reports the proximal alpha1-alpha2 loop as a second activation site in Bak and in mitochondrial Bax. PMID: 27217060
    3. The proapoptotic BCL-2 proteins BAX and BAK can commit a cell to its programmed death by permeabilizing the outer mitochondrial membrane and subsequent initiation of the caspase cascade. (Review) PMID: 28676391
    4. Data suggest that ECAD, STAT3, Bak, and Bcl-xL are expressed in affected endometrial tissues of women with endometrioid adenocarcinoma depending on neoplasm staging and cell differentiation. This study was conducted using immunohistochemistry of surgically resected tissues. (ECAD = E-cadherin; STAT3 = signal transducer and activator of transcription 3 protein; Bcl-xL = BCL2 associated agonist of cell death) PMID: 28937296
    5. This comprehensive survey showed that in each Bak dimer the N-termini are fully solvent-exposed and mobile, the core is highly structured, and the C-termini are flexible but restrained by their contact with the membrane. PMID: 28182867
    6. The BAK1/BCL2 ratio was positively correlated with the results of audiometric tests. Our results indicate that BAK-mediated apoptosis may be a core mechanism in the progression of age-related hearing impairment in humans PMID: 27555755
    7. UMI-77 enhances TRAIL-induced apoptosis by unsequestering Bim and Bak, which provides a novel therapeutic strategy for the treatment of gliomas. PMID: 28337703
    8. after the induction of apoptosis, Bak switches from its association with Mtx2 and VDAC2 to a closer association with Mtx1. PMID: 27845183
    9. Conversion of Bim-BH3 from Activator to Inhibitor of Bak through Structure-Based Design. PMID: 29149594
    10. The results strongly suggest that the direct apoptosis-activation activities of Bid, Bim, Puma, and p53 are not essential for activating Bax/Bak once the anti-apoptotic Bcl-2 proteins are neutralized. PMID: 27310874
    11. Studied BAK1, SPRY4 and GAB2 SNPs in pediatric germ cell tumors(GCT); found a variant in SPRY4 was associated with reduced risk of GCT; a variant in BAK1 was positively associated with GCT with a strong estimated effect for testis tumors; and a SNP in GAB2 was associated with increased risk for GCT. PMID: 28295819
    12. These results not only establish Bok as a Bak- and Bax-independent apoptosis inducer, but also suggest a potential impact of Bok expression in ovarian cancer therapy. PMID: 27076518
    13. The low-level constitutive production of platelets caused by the G allele of rs5745568 in BAK1 protein seems to increase the risk of bleeding in dengue infection PMID: 27401010
    14. the expression of Bak1 was downregulated in CRC tumor tissues and was reversely correlated with the expression of miR410, which provided further support that Bak1 was regulated by miR410. PMID: 27177325
    15. Low expression of BAX is associated with docetaxel resistance in gastric cancer. PMID: 26486506
    16. Polymorphisms of KITLG, SPRY4, and BAK1 genes in patients with testicular germ cell tumors and individuals with infertility associated with AZFc deletion of the Y chromosome PMID: 28064312
    17. Different selenium concentrations had varying effects on BAK1 and APAF1 levels. APAF1 may play an important role in the pathogenesis of KBD PMID: 26179084
    18. Findings argue for auto-activation of Bak in the absence of anti-apoptotic Bcl-2 proteins and provide evidence of profound differences in the activation of Bax and Bak. PMID: 26610208
    19. LTX-315 kills cancer cells through Bax/Bak-regulated mitochondrial membrane permeabilization PMID: 26378049
    20. E6 proteins of human papillomavirus types 6 and 11 are able to protect keratinocytes from apoptosis via Bak degradation. PMID: 26743580
    21. Bak apoptotic pores involve a flexible C-terminal region and juxtaposition of the C-terminal transmembrane domains. PMID: 25744027
    22. Low expression of pro-apoptotic Bak protein in in Waldenstrom macroglobulinemia. PMID: 25893290
    23. Report shows that high Bak expression is associated with the favorable overall survival rates of breast cancer patients. PMID: 26406239
    24. alpha1 dissociation is a key step in unfolding Bak into three major components, the N terminus, the core (alpha2-alpha5) and the latch (alpha6-alpha8) that is required for apoptosis. PMID: 25880232
    25. the BH3 mimetic ABT-737 induces autophagy through a BAX and BAK1-independent mechanism that likely involves disruption of BECN1 binding to antiapoptotic BCL2 family members PMID: 25715028
    26. Data with full-length proteins indicate that most BH3-only proteins can directly activate both Bak and Bax. PMID: 25906158
    27. Puma is the major mediator of virus-induced Bax/Bak activation and mitochondrial membrane permeabilization induction. PMID: 26030884
    28. Data show that mitochondrial X-linked inhibitor of apoptosis protein (XIAP) entry requires apoptosis regulatory proteins Bax or Bak through mitochondrial permeabilization and Smac/DIABLO protein degradation. PMID: 26134559
    29. BMX directly inhibits a core component of the intrinsic apoptosis machinery opens opportunities to improve the efficacy of existing chemotherapy by potentiating BAK-driven cell death in cancer cells. PMID: 25649765
    30. high BAK expression correlates with sensitivity of clinical acute myelogenous leukemia to chemotherapy, whereas low BAK levels correlate with resistance and relapse PMID: 26494789
    31. Motifs of VDAC2 required for mitochondrial Bak import and tBid-induced apoptosis. PMID: 26417093
    32. By down-regulating Bak, P53, P21, BRCA1, BCL-Xl. PMID: 25773855
    33. Results show that in thyroid tumours and cell lines, VDAC2 is upregulated and BAK1 downregulated. Also, transient knockdown of VDAC2 promoted upregulation of the BAK1 expression, and increased susceptibility to sorafenib treatment. PMID: 25617717
    34. Chk1 activity is required for BAK multimerization in association with PUMA during mitochondrial apoptosis PMID: 25012639
    35. Studies show that necrosis requires Bcl-2-associated protein x (Bax) and Bcl-2 homologues antagonist/killer (Bak), which can regulate the permeability characteristics of the outer mitochondrial membrane. PMID: 25999420
    36. G-Rh2 causes rapid and dramatic translocation of both Bak and Bax, which subsequently triggers mitochondrial cytochrome c release and consequent caspase activation. PMID: 23443079
    37. Data show that E3 ubiquitin-protein ligase HERC1 interacts with bcl-2 homologous antagonist-killer protein BAK in HPV5 E6-expressing cells that have been damaged by UV. PMID: 25408501
    38. Data show that proto-oncogene protein ERBB3 knockdown resulted in cell cycle arrest and activation of Bak and Bax-dependent apoptosis. PMID: 24970817
    39. The Bak and Bax genes expressions were analyzed in 23 breast cancer patients. PMID: 24672785
    40. The mitochondrial metalloprotease OMA1 was activated in a Bax- and Bak-dependent fashion. PMID: 25275009
    41. Helices contribute to mitochondrial outer membrane perforation in that oligomers Bak alpha5 (like Bax alpha5) remain part of the protein core and a membrane-impermeable cysteine reagent labels cysteines placed at many positions in alpha5 and alpha6 of both Bak and Bax. PMID: 25228770
    42. enhanced efficacy of combination of mdivi-1 and death ligands is not dependent on the originally reported target of mdivi-1, Drp1, and is also not dependent on the two important pro-apoptotic Bcl-2 family proteins Bax and Bak PMID: 25446129
    43. the reduction of Bax shuttling to the level of Bak retrotranslocation results in full Bax toxicity even in absence of apoptosis induction. PMID: 25378477
    44. Clitocine may activate Bak by disrupting the interaction between Mcl-1. PMID: 25304383
    45. Bak interacts with Mtx2 together with VDAC2 in resting cells and with Mtx1 upon induction of apoptosis. PMID: 24794530
    46. This progress has resolved longstanding controversies, but has also challenged established theories in the apoptosis field, it focus on the recent progress made in characterizing the proapoptotic Bax and Bak. PMID: 24162660
    47. Caspase 8 cleavage by HIV protease activates BAK, enabling HIV to kill infected T cells. PMID: 25246614
    48. Data shows that Bak undergoes a conformational change similar to that of Bax upon activation. PMID: 25175025
    49. our data strongly support an important role for miR-125b on conferring TMZ resistance through targeting Bak1 expression. PMID: 24643683
    50. s demonstrate that during vaccinia virus infection, engagement of Bim and Bak by F1L is crucial for subversion of host cell apoptosis. PMID: 24850748

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  • 亚细胞定位：
    Mitochondrion outer membrane; Single-pass membrane protein.
  • 蛋白家族：
    Bcl-2 family
  • 组织特异性：
    Expressed in a wide variety of tissues, with highest levels in the heart and skeletal muscle.
  • 数据库链接：

    HGNC: 949

    OMIM: 600516

    KEGG: hsa:578

    STRING: 9606.ENSP00000353878

    UniGene: Hs.485139