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Merck
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Key Documents

MABT322

Sigma-Aldrich

Anti-DDR2 Antibody, clone 2B12.1

clone 2B12.1, from mouse

Sinónimos:

Discoidin domain-containing receptor 2, CD167 antigen-like family member B, CD167b, Discoidin domain receptor 2, Discoidin domain-containing receptor tyrosine kinase 2, Neurotrophic tyrosine kinase, receptor-related 3, Receptor protein-tyrosine kinase TK

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

2B12.1, monoclonal

species reactivity

human, mouse, rat

technique(s)

immunohistochemistry: suitable
western blot: suitable

isotype

IgG2aκ

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... TKT(7086)

General description

Discoidin domain-containing receptor 2 (EC 2.7.10.1; UniProt Q16832; also known as CD167 antigen-like family member B, CD167b, Discoidin domain receptor 2, Discoidin domain-containing receptor tyrosine kinase 2, Neurotrophic tyrosine kinase, receptor-related 3, Receptor protein-tyrosine kinase TKT, Tyrosine-protein kinase TYRO10) is encoded by the DDR2 (also known as NTRKR3, TKT, TYRO10) gene (Gene ID 4921) in human. Discoidin domain-containing receptors (DDRs) belong to the superfamily of transmembrane receptor tyrosine kinases (RTKs). DDRs are distinguished from other RTKs by their extracellular discoidin motif and their utilization of collagens as internal ligands. While DDR1 binds essentially all types of collagens, DDR2 shows a preference for type I, II and III fibrillar collagens, and nonfibrillar type X collagen. DDR1 is widely expressed in epithelial cells in lung, kidney, colon, and brain, whereas DDR2 is primarily expressed in mesenchymal cells including fibroblasts, myofibroblasts, smooth muscle cells, and chondrocytes in kidney, skin, lung, heart, and connective tissues. DDRs are important mediators of fundamental cellular processes, such as proliferation, survival, differentiation, adhesion and matrix remodeling, their dysregulations are reported to cause a number of human diseases, including fibrotic disorders, atherosclerosis and cancer. DDR2 is initially produced with a signal peptide sequence (a.a. 1-21), the removal of which yields the mature protein with an extracellular region (a.a. 22-399), followed by a transmembrane segment (a.a. 400-421) and a cytoplasmic region (a.a. 422-855) that harbors the kinase domain (a.a. 563-849).

Immunogen

GST-tagged recombinant human DDR2 internal fragment.

Application

This Anti-DDR2 Antibody, clone 2B12.1 is validated for use in Western Blotting, Immunohistochemistry for the detection of DDR2.
Western Blotting Analysis: 1.0 µg/mL of this antibody detected DDR2 in 10 µg of rat L6 myoblast and human HeLa cell lysates.
Immunohistochemistry Analysis: A 1:250 dilution from a representative lot detected DDR2 in human lung and kidney tissue sections.

Quality

Evaluated by Western Blotting in NIH3T3 cell lysate.

Western Blotting Analysis: 1.0 µg/mL of this antibody detected DDR2 in 10 µg of NIH3T3 cell lysate.

Target description

~107/115 kDa observed. Target band(s) appears larger than the calculated molecular weight of 96.74 kDa due to glycosylation. A doublet banding pattern is often seen with the lower band representing less glycosylated DDR2 species.

Physical form

Format: Purified

Other Notes

Concentration: Please refer to lot specific datasheet.

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Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Xiujie Sun et al.
Nature, 599(7886), 673-678 (2021-11-05)
Immune exclusion predicts poor patient outcomes in multiple malignancies, including triple-negative breast cancer (TNBC)1. The extracellular matrix (ECM) contributes to immune exclusion2. However, strategies to reduce ECM abundance are largely ineffective or generate undesired outcomes3,4. Here we show that discoidin
Mereena George Ushakumary et al.
PloS one, 14(12), e0225911-e0225911 (2019-12-06)
Collagen accumulation and remodeling in the vascular wall is a cardinal feature of vascular fibrosis that exacerbates the complications of hypertension, aging, diabetes and atherosclerosis. With no specific therapy available to date, identification of mechanisms underlying vascular fibrogenesis is an

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