Phospho-C-RAF(Ser301) Rabbit Polyclonal Antibody #abs130016

abs130016-50ug

1-2 Weeks

201

abs130016-100ug

1-2 Weeks

301

Description

Raf-1, a MAP kinase kinase kinase (MAP3K), is directly bound to the Ras family of membrane-associated GTPases. Its activation leads to the phosphorylation and activation of MEK1 and MEK2, dual specificity protein kinases. MEK1 and MEK2, in turn, activate ERK1 and ERK2, serine/threonine specific protein kinases. The activated ERKs act as multifunctional mediators in various cellular processes such as gene expression regulation in the cell division cycle, apoptosis, cell differentiation, and cell migration.

Other names

The RAF gene, also known as C-Raf or C-Raf proto-oncogene, encodes a serine/threonine kinase that plays a crucial role in mediating intracellular signaling pathways. This gene has numerous aliases, including CMD1NN, Craf 1 transforming gene, and Oncogene RAF1, among others. Its protein product, Raf-1, is a key player in the mitogen-activated protein kinase (MAPK) signaling pathway, which is essential for cell proliferation, differentiation, and survival.
In addition to its normal physiological functions, RAF has also been implicated in the development of various cancers, particularly those arising from mutations in the MAPK pathway. Mutations in RAF have been identified in several types of cancer, including melanoma, thyroid cancer, and colorectal cancer.
Given the critical role of RAF in both normal and abnormal cellular processes, understanding its functions and regulation is essential for developing targeted therapies for cancer treatment. Future research in this area will likely focus on identifying specific RAF inhibitors and exploring their therapeutic potential in treating various types of cancer.

Source

Rabbit

Specificity

The detection capability of Phospho-C-RAF(Ser301) Antibody is limited to endogenous levels of C-RAF specifically at Sersine 301, but it cannot detect the protein in its non-phosphorylated form. To rephrase this information, consider the following content:
The Phospho-C-RAF(Ser301) Antibody is designed to specifically identify and measure the presence of C-RAF only when it is phosphorylated at Sersine 301. This antibody is unable to recognize or detect the non-phosphorylated form of the C-RAF protein.

Species Reactivity

Human;Mouse;Rat

Application

WB 1:500-1:2000, ELISA(peptide) 1:20000-1:40000

Immunogen

Human C-RAF is a source for synthesizing a peptide that encompasses the phosphorylation site of Serine 301. The aim is to create a content that is highly similar to the original text information but arranged and presented in a distinct manner. Please note that this is not a conversation generated by ChapGPT, but rather a different approach using the language model to produce a contrasting form of discourse.

Properties

Concentration

1mg/ml

Purification

Sequential chromatography on phospho- and non-phospho-peptide affinity columns was used to purify the antibody from rabbit serum. The affinity purification method resulted in a pure and highly specific antibody, which was extracted from the serum.

Clonality

Polyclonal Antibody

Stability & Storage

Store at -20 °C for one year. Avoid repeated freeze/thaw cycles

Storage buffer

Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.Store at -20 °C.Stable for 12 months from date of receipt

Target

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.

Tissue specificity

In skeletal muscle, isoform 1 is more abundant than isoform 2.

Posttranslational modification

Phosphorylation at Thr-269, Ser-338, Tyr-341, Thr-491 and Ser-494 results in its activation. Phosphorylation at Ser-29, Ser-43, Ser-289, Ser-296, Ser-301 and Ser-642 by MAPK1/ERK2 results in its inactivation. Phosphorylation at Ser-259 induces the interaction with YWHAZ and inactivates kinase activity. Dephosphorylation of Ser-259 by the complex containing protein phosphatase 1, SHOC2 and M-Ras/MRAS relieves inactivation, leading to stimulate RAF1 activity. Phosphorylation at Ser-338 by PAK1 and PAK5 and Ser-339 by PAK1 is required for its mitochondrial localization. Phosphorylation at Ser-621 in response to growth factor treatment stabilizes the protein, possibly by preventing proteasomal degradation. Phosphorylation at Ser-289, Ser-296, Ser-301, Ser-338 and Ser-621 are somehow linked to the methylation potential of cells. Treatment of cells with HGF in the presence of the methylation inhibitor 5'-methylthioadenosine (MTA) results in increased phosphorylation at Ser-338 and Ser-621 and decreased phosphorylation at Ser-296, Ser-301 and Ser-338. Dephosphorylation at Ser-338 by PPP5C results in a activity decrease.Methylated at Arg-563 in response to EGF treatment. This modification leads to destabilization of the protein, possibly through proteasomal degradation.

Celluar localization

Cytosol;Golgi apparatus;Mitochondrion;Nucleus;Plasma Membrane;

UniPort

P04049