BLNK Antibody [L16M19]

Catalog No.: F5052

Application: Reactivity: Human, Mouse

Lane 1: Ramos, Lane 2: Raji, Lane 3: Daudi, Lane 4: A20

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代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:1000 IP1:50 IHC1:250 IF1:800-1:1600 FCM1:50

Application
WB, IP, IHC, IF, FCM

Source
Rabbit Monoclonal Antibody

Reactivity
Human, Mouse

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
68 kDa, 70 kDa

Datasheet & SDS

生物学的記述

Specificity
BLNK Antibody [L16M19] detects endogenous levels of total BLNK protein.

Clone
L16M19

Synonym(s)
B-cell linker protein; B-cell adapter containing a SH2 domain; B-cell adapter containing a Src homology 2 domain; Cytokine receptor-binding link protein; SLP-65; SLP65; BLNK; BASH; LY57

Background
BLNK serves as an adaptor protein in B lymphocytes, linking BCR-associated kinases to downstream effectors without intrinsic enzymatic activity. It features multiple tyrosine motifs at the N-terminus that conform to SH2-binding consensus sequences and a C-terminal SH2 domain. Upon BCR engagement, Syk phosphorylates BLNK at several tyrosine residues, creating docking sites for SH2 domains of BTK, PLCγ2, Vav, Grb2, and NCK, while BLNK's SH2 domain binds tyrosine-phosphorylated targets like HPK1 to recruit them into the signaling complex. Phosphorylated BLNK facilitates Syk access to BTK by positioning BTK's SH2 domain onto its phosphotyrosines, enabling Syk-mediated transphosphorylation of BTK at the activation loop tyrosine and enhancing BTK kinase activity essential for PLCγ2 phosphorylation and IP3-mediated calcium mobilization. BLNK coordinates activation of MAP kinase cascades through Vav-Rac1-JNK and Grb2-Sos-Ras-ERK pathways, NF-κB nuclear translocation for survival and proliferation, and PI3K-Akt signaling for metabolic support during B cell responses. BLNK supports pre-BCR-induced PLCγ2 activation and calcium influx critical for proliferation and differentiation from large cycling to small resting stages, while MAP kinase and PI3K pathways proceed independently. Absence of BLNK impairs calcium signaling and PLCγ2 phosphorylation yet permits Syk-Shc-Ras-ERK and AKT activation post-pre-BCR ligation. Dysregulated BLNK expression underlies partial B cell developmental blocks at pro-B/pre-B transition and predisposes to pre-B acute lymphoblastic leukemia through unchecked proliferation.

Background

BLNK serves as an adaptor protein in B lymphocytes, linking BCR-associated kinases to downstream effectors without intrinsic enzymatic activity. It features multiple tyrosine motifs at the N-terminus that conform to SH2-binding consensus sequences and a C-terminal SH2 domain. Upon BCR engagement, Syk phosphorylates BLNK at several tyrosine residues, creating docking sites for SH2 domains of BTK, PLCγ2, Vav, Grb2, and NCK, while BLNK's SH2 domain binds tyrosine-phosphorylated targets like HPK1 to recruit them into the signaling complex. Phosphorylated BLNK facilitates Syk access to BTK by positioning BTK's SH2 domain onto its phosphotyrosines, enabling Syk-mediated transphosphorylation of BTK at the activation loop tyrosine and enhancing BTK kinase activity essential for PLCγ2 phosphorylation and IP3-mediated calcium mobilization. BLNK coordinates activation of MAP kinase cascades through Vav-Rac1-JNK and Grb2-Sos-Ras-ERK pathways, NF-κB nuclear translocation for survival and proliferation, and PI3K-Akt signaling for metabolic support during B cell responses. BLNK supports pre-BCR-induced PLCγ2 activation and calcium influx critical for proliferation and differentiation from large cycling to small resting stages, while MAP kinase and PI3K pathways proceed independently. Absence of BLNK impairs calcium signaling and PLCγ2 phosphorylation yet permits Syk-Shc-Ras-ERK and AKT activation post-pre-BCR ligation. Dysregulated BLNK expression underlies partial B cell developmental blocks at pro-B/pre-B transition and predisposes to pre-B acute lymphoblastic leukemia through unchecked proliferation.

References
[1] Baba Y, et al. Proc Natl Acad Sci U S A. 2001 Feb 27;98(5):2582-6. [2] Fu C, et al. Immunity. 1998 Jul;9(1):93-103.

PVDFメンブレン孔径参考表

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%