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Rabbit Anti-SLK/BF594 Conjugated antibody (bs-3519R-BF594)
訂購熱線:400-901-9800
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產品編號 bs-3519R-BF594
英文名稱 Rabbit Anti-SLK/BF594 Conjugated antibody
中文名稱 BF594標記的酪氨酸蛋白激酶Fyn/同步原癌基因抗體
別    名 Fyn; C syn protooncogene; FYN oncogene related to SRC FGR YES; MGC45350; OKT3 induced calcium influx regulator; P59 FYN; Protein tyrosine kinase fyn; Proto oncogene tyrosine protein kinase fyn; Protooncogene Syn; SLK; Src like kinase; Src yes related novel gene; Src/yes related novel gene;SYN; Tyrosine kinase p59fyn T; Tyrosine kinase p59fyn(T); FYN_HUMAN; Tyrosine-protein kinase Fyn; Proto-oncogene Syn; Proto-oncogene c-Fyn; Src-like kinase; p59-Fyn.  
規格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領域 腫瘤  免疫學  神經生物學  信號轉導  細胞凋亡  轉錄調節因子  激酶和磷酸酶  細胞膜受體  Alzheimer's  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應 Human, Mouse,  (predicted: Rat, Chicken, Dog, Pig, Cow, Rabbit, )
產品應用 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 59kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human SLK
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
產品介紹 background:
This gene is a member of the protein-tyrosine kinase oncogene family. It encodes a membrane-associated tyrosine kinase that has been implicated in the control of cell growth. The protein associates with the p85 subunit of phosphatidylinositol 3-kinase and interacts with the fyn-binding protein. Alternatively spliced transcript variants encoding distinct isoforms exist. [provided by RefSeq, Jul 2008]

Function:
Non-receptor tyrosine-protein kinase that plays a role in many biological processes including regulation of cell growth and survival, cell adhesion, integrin-mediated signaling, cytoskeletal remodeling, cell motility, immune response and axon guidance. Inactive FYN is phosphorylated on its C-terminal tail within the catalytic domain. Following activation by PKA, the protein subsequently associates with PTK2/FAK1, allowing PTK2/FAK1 phosphorylation, activation and targeting to focal adhesions. Involved in the regulation of cell adhesion and motility through phosphorylation of CTNNB1 (beta-catenin) and CTNND1 (delta-catenin). Regulates cytoskeletal remodeling by phosphorylating several proteins including the actin regulator WAS and the microtubule-associated proteins MAP2 and MAPT. Promotes cell survival by phosphorylating AGAP2/PIKE-A and preventing its apoptotic cleavage. Participates in signal transduction pathways that regulate the integrity of the glomerular slit diaphragm (an essential part of the glomerular filter of the kidney) by phosphorylating several slit diaphragm components including NPHS1, KIRREL and TRPC6. Plays a role in neural processes by phosphorylating DPYSL2, a multifunctional adapter protein within the central nervous system, ARHGAP32, a regulator for Rho family GTPases implicated in various neural functions, and SNCA, a small pre-synaptic protein. Participates in the downstream signaling pathways that lead to T-cell differentiation and proliferation following T-cell receptor (TCR) stimulation. Also participates in negative feedback regulation of TCR signaling through phosphorylation of PAG1, thereby promoting interaction between PAG1 and CSK and recruitment of CSK to lipid rafts. CSK maintains LCK and FYN in an inactive form. Promotes CD28-induced phosphorylation of VAV1.

Subunit:
Interacts (via its SH3 domain) with PIK3R1 and PRMT8. Interacts with FYB, PAG1, and SH2D1A. Interacts with CD79A (tyrosine-phosphorylated form); the interaction increases FYN activity. Interacts (via SH2 domain) with CSF1R (tyrosine phosphorylated). Interacts with TOM1L1 (phosphorylated form). Interacts with KDR (tyrosine phosphorylated). Interacts (via SH3 domain) with KLHL2 (via N-terminus). Interacts with SH2D1A and SLAMF1. Interacts (via its SH3 domain) with HEV ORF3 protein. Interacts with ITCH; the interaction phosphorylates ITCH and negatively regulates its activity. Interacts with FASLG. Interacts with RUNX3. Interacts with KIT. Interacts with EPHA8; possible downstream effector of EPHA8 in regulation of cell adhesion. Interacts with PTK2/FAK1; this interaction leads to PTK2/FAK1 phosphorylation and activation. Interacts with CAV1; this interaction couples integrins to the Ras-ERK pathway.

Subcellular Location:
Cytoplasm. Nucleus. Cell membrane. Note=Present and active in lipid rafts. Palmitoylation is crucial for proper trafficking.

Tissue Specificity:
Isoform 1 is highly expressed in the brain. Isoform 2 is expressed in cells of hemopoietic lineages, especially T lymphocytes.

Post-translational modifications:
Autophosphorylated at Tyr-420. Phosphorylation on the C-terminal tail at Tyr-531 by CSK maintains the enzyme in an inactive state. PTPRC/CD45 dephosphorylates Tyr-531 leading to activation. ultraviolet B (UVB) strongly increase phosphorylation at Thr-12 and kinase activity, and promotes translocation from the cytoplasm to the nucleus. Dephosphorylation at Tyr-420 by PTPN2 negatively regulates T-cell receptor signaling.
Palmitoylation at Cys-3 and Cys-6 regulates subcellular location.

Similarity:
Belongs to the protein kinase superfamily. Tyr protein kinase family. SRC subfamily.
Contains 1 protein kinase domain.
Contains 1 SH2 domain.
Contains 1 SH3 domain.

Database links:

Entrez Gene: 2534 Human

Entrez Gene: 14360 Mouse

Entrez Gene: 25150 Rat

Omim: 137025 Human

SwissProt: P06241 Human

SwissProt: P39688 Mouse

SwissProt: Q62844 Rat

Unigene: 390567 Human

Unigene: 4848 Mouse

Unigene: 19361 Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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