E. coli biotin ligase
(BirA) is highly specific in covalently attaching biotin to the 15
amino
acid AviTag peptide. This recombinant protein was biotinylated in
vivo
by AviTag-BirA technology, which method is BriA catalyzes amide
linkage
between the biotin and the specific lysine of the AviTag.
The tag type will
be
determined during production process. If you have specified tag
type, please tell us and we will develop the specified tag
preferentially.
產品提供形式:
Lyophilized
powder
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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.
復溶:
We recommend that this vial be briefly centrifuged
prior
to opening to bring the contents to the bottom. Please reconstitute
protein in deionized sterile water to a concentration of 0.1-1.0
mg/mL.We recommend to add 5-50% of glycerol (final concentration)
and
aliquot for long-term storage at -20℃/-80℃. Our default final
concentration of glycerol is 50%. Customers could use it as
reference.
儲存條件:
Store at -20°C/-80°C upon receipt, aliquoting is
necessary for
mutiple use. Avoid repeated freeze-thaw cycles.
保質期:
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.
貨期:
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.
注意事項:
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet :
Please contact us to get it.
產品評價
靶點詳情
功能:
DNA repair protein that may operate in a postreplication repair or a cell cycle checkpoint function. May be implicated in interstrand DNA cross-link repair and in the maintenance of normal chromosome stability. Upon IFNG induction, may facilitate STAT1 activation by recruiting STAT1 to IFNGR1.
基因功能參考文獻:
Genetic deletion of Fancc blocks the autophagic clearance of viruses (virophagy) and increases susceptibility to lethal viral encephalitis. Fanconi anemia complementation group C (FANCC) protein interacts with Parkin, is required in vitro and in vivo for clearance of damaged mitochondria, and decreases mitochondrial reactive oxygen species (ROS) production and inflammasome activation. PMID: 27133164
Data show that Fanconi anemia, complementation group C protein knockout (Fancc -/-) mice develop hematopoietic chromosomal instability followed by leukemia in an age-dependent manner. PMID: 26860989
Loss of Fancc Impairs Antibody-Secreting Cell Differentiation in Mice through Deregulating the Wnt Signaling Pathway PMID: 26895835
Combined deficiency of Foxo3a and Fancc or Fancd2 not only impairs the self-renewal capacity but also markedly increases the apoptosis of neural stem and progenitor cells (NSPCs), leading to defective neurogenesis. PMID: 24483844
Using mice deficient in both Mus81 and the FA pathway protein FancC, we show both proteins cooperate in parallel pathways, as concomitant loss of FancC and Mus81 triggered cell-type-specific proliferation arrest, apoptosis and DNA damage accumulation in utero. PMID: 25056314
Loss of FANCC leads to a drastic increase in stalled/collapsed forks in cells carrying an Mcm4 missense mutation. PMID: 24589582
FANCC is most likely to be critical for resistance to DNA cross-linking drug-induced DNA damage in cells transformed by JAK2 V617F mutant. PMID: 23838005
Data indicate that IL-1beta overproduction from FANCC-deficient macrophages is p38 dependent. PMID: 24046015
Loss of FANCC expression results in an impaired emergency granulopoiesis response in a transgenic mouse model of Fanconi anemia. PMID: 23925293
Compromised hematopoiesis in Fancc(-/-) animals is developmentally programmed and does not arise de novo in bone marrow. PMID: 23315168
Double-mutant Fancc(-/-);Fancg(-/-) mice develop spontaneous hematologic sequelae including bone marrow failure, acute myeloid leukemia, myelodysplasia and complex random chromosomal abnormalities that the single-mutant mice do not. PMID: 20606166
Fancc deficiency accelerates telomere shortening during high turnover of hematopoietic cells and promotes telomere recombination initiated by short telomeres. PMID: 20022886
whereas Fancc-/- mice failed to form hematopoietic or solid malignancies, mice mutant at both Fancc and Trp53 developed tumors more rapidly than mice mutant at Trp53 alone. PMID: 12855557
Fancc mutations result in a subtle immunological defect owing to the failure of FANCC to normally support Janus kinase/STAT signaling, such that differentiation of Fancc-/- CD4+ T cells into the Th1 subset is impaired in Fancc-deficient mice. PMID: 15356134
the intrinsic defects in the genomic stability of Fancc(-/-) stem/progenitor cells provide a selective pressure for cells that are resistant to apoptosis and have a propensity for the evolution to clonal hematopoiesis and malignancy PMID: 15644418
predisposition of Fancc-/- hematopoietic progenitors to apoptosis is mediated in part through altered redox regulation and apoptosis signal-regulating kinase 1 hyperactivation PMID: 16109778
Data suggest that TNF-alpha exposure creates an environment in which somatically mutated preleukemic stem cell clones are selected and from which unaltered TNF-alpha-hypersensitive Fancc-/- stem cells are purged. PMID: 17960249
Short-term transduction of c-kit(+) cells with a foamyviral vector is sufficient for functional correction of a stem cell phenotype in a murine Fanconi anemia model. PMID: 18684868
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亞細胞定位:
Nucleus. Cytoplasm. Note=The major form is nuclear. The minor form is cytoplasmic.