This webpage contains legacy information. The product is either no longer available from the supplier or has been delisted at Labome.
product summary
company name :
Bioss
product type :
antibody
product name :
c-Raf(Tyr341) Polyclonal Antibody
catalog :
bs-5650R
quantity :
100 ul
clonality :
polyclonal
host :
domestic rabbit
conjugate :
nonconjugated
reactivity :
human
application :
western blot, immunocytochemistry, immunohistochemistry - paraffin section
product information
sku :
bs-5650R
name :
c-Raf(Tyr341) Polyclonal Antibody
category :
Primary Antibody
conjugation :
Unconjugated
host :
Rabbit
target protein :
c-Raf Tyr341
modification :
Phosphorylation
modification site :
Tyr341
clonality :
Polyclonal
isotype :
IgG
concentration :
1ug/ul
public immunogen range :
325-375/648
subcellular locations :
Cytoplasm, Nucleus, Mitochondrion, Cell membrane
source :
KLH conjugated synthetic phosphopeptide derived from human c-Raf around the phosphorylation site of Tyr341
gene id link :
Entrez Gene: 5894
swiss prot :
P04049
swiss prot link :
Swiss Prot: P04049
applications :
WB, IHC-P, IF(IHC-P)
applications with dilutions :
WB(1:100-1000), IHC-P(1:100-500), IF(IHC-P)(1:50-200)
cross reactive species :
Human
size :
100 ul
background :
Serine/threonine-protein kinase that acts as a regulatory link between the membrane-associated Ras GTPases and the MAPK/ERK cascade, and this critical regulatory link functions as a switch determining cell fate decisions including proliferation, differentiation, apoptosis, survival and oncogenic transformation. RAF1 activation initiates a mitogen-activated protein kinase (MAPK) cascade that comprises a sequential phosphorylation of the dual-specific MAPK kinases (MAP2K1/MEK1 and MAP2K2/MEK2) and the extracellular signal-regulated kinases (MAPK3/ERK1 and MAPK1/ERK2). The phosphorylated form of RAF1 (on residues Ser-338 and Ser-339, by PAK1) phosphorylates BAD/Bcl2-antagonist of cell death at 'Ser-75'. Phosphorylates adenylyl cyclases: ADCY2, ADCY5 and ADCY6, resulting in their activation. Phosphorylates PPP1R12A resulting in inhibition of the phosphatase activity. Phosphorylates TNNT2/cardiac muscle troponin T. Can promote NF-kB activation and inhibit signal transducers involved in motility (ROCK2), apoptosis (MAP3K5/ASK1 and STK3/MST2), proliferation and angiogenesis (RB1). Can protect cells from apoptosis also by translocating to the mitochondria where it binds BCL2 and displaces BAD/Bcl2-antagonist of cell death. Regulates Rho signaling and migration, and is required for normal wound healing. Plays a role in the oncogenic transformation of epithelial cells via repression of the TJ protein, occludin (OCLN) by inducing the up-regulation of a transcriptional repressor SNAI2/SLUG, which induces down-regulation of OCLN. Restricts caspase activation in response to selected stimuli, notably Fas stimulation, pathogen-mediated macrophage apoptosis, and erythroid differentiation.
purification :
Purified by Protein A.
storage :
Aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Store at -20°C for 12 months.
synonyms :
NS5; CRAF; Raf-1; c-Raf; CMD1NN; RAF proto-oncogene serine/threonine-protein kinase; Proto-oncogene c-RAF; RAF1; RAF
lead time :
3 to 5 business days.
company information
Bioss
500 West Cummings Park
Suite 6500
Woburn, MA 01801
Suite 6500
Woburn, MA 01801
info@biossusa.com
http://biossusa.com800-501-7654
headquarters: USA
Bioss Inc is a leading antibody developer and manufacturer with state of the art technologies. We have developed over 11,000 antigens/primary antibodies and more than 130,000 derived products including fluorochrome conjugated antibodies. In addition to reliable loading control and tag antibodies, our catalog includes over 1000 specific antibodies recognizing proteins with phosphorylation, acetylation, or methylation modifications. Our company promises fast delivery with strong, top quality scientific support. Bioss Inc is located in the greater Boston area of Massachusetts, the center of the world's largest and fastest growing biotech community.
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