CEACAM8 Antibody - #DF10151

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Product: CEACAM8 Antibody
Catalog: DF10151
Description: Rabbit polyclonal antibody to CEACAM8
Application: WB IHC IF/ICC
Reactivity: Human, Rat
Mol.Wt.: 38 kDa; 38kD(Calculated).
Uniprot: P31997
RRID: AB_2840730

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Related Downloads
MS Report
HPLC Report
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:1000-3000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Rat
Clonality:
Polyclonal
Specificity:
CEACAM8 Antibody detects endogenous levels of total CEACAM8.
RRID:
AB_2840730
Cite Format: Affinity Biosciences Cat# DF10151, RRID:AB_2840730.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

Carcinoembryonic antigen CGM6; Carcinoembryonic antigen gene family member 6; Carcinoembryonic antigen related cell adhesion molecule 8; Carcinoembryonic antigen-related cell adhesion molecule 8; CD 66b; CD 67; CD66b; CD66b antigen; CD67; CD67 antigen; CEACAM 8; CEACAM8; CEAM8_HUMAN; CGM 6; CGM6; NCA 95; NCA95; Non-specific cross-reacting antigen NCA-95; Nonspecific cross reacting antigen NCA 95; Nonspecific cross reacting antigen NCA95;

Immunogens

Immunogen:
Uniprot:

P31997(CEAM8_HUMAN) >>Visit HPA database.

Gene(ID):
CEACAM8(1088)
Expression:
P31997 CEAM8_HUMAN:

Expressed in leukocytes of chronic myeloid Leukemia patients and bone marrow.

Sequence:
MGPISAPSCRWRIPWQGLLLTASLFTFWNPPTTAQLTIEAVPSNAAEGKEVLLLVHNLPQDPRGYNWYKGETVDANRRIIGYVISNQQITPGPAYSNRETIYPNASLLMRNVTRNDTGSYTLQVIKLNLMSEEVTGQFSVHPETPKPSISSNNSNPVEDKDAVAFTCEPETQNTTYLWWVNGQSLPVSPRLQLSNGNRTLTLLSVTRNDVGPYECEIQNPASANFSDPVTLNVLYGPDAPTISPSDTYYHAGVNLNLSCHAASNPPSQYSWSVNGTFQQYTQKLFIPNITTKNSGSYACHTTNSATGRNRTTVRMITVSDALVQGSSPGLSARATVSIMIGVLARVALI

PTMs - P31997 As Substrate

Site PTM Type Enzyme
Y120 Phosphorylation
K126 Methylation
N288 N-Glycosylation
S296 Phosphorylation

Research Backgrounds

Function:

Cell surface glycoprotein that plays a role in cell adhesion in a calcium-independent manner. Mediates heterophilic cell adhesion with other carcinoembryonic antigen-related cell adhesion molecules, such as CEACAM6. Heterophilic interaction with CEACAM8 occurs in activated neutrophils.

PTMs:

Glycosylated.

Subcellular Location:

Cell membrane>Lipid-anchor. Cell surface.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Expressed in leukocytes of chronic myeloid Leukemia patients and bone marrow.

Subunit Structure:

Monomer. Heterodimer with CEACAM6; heterodimerizes via its Ig-like V-type domain.

Family&Domains:

The N-terminus Ig-like V-type domain is necessary for heterophilic intercellular adhesion.

Belongs to the immunoglobulin superfamily. CEA family.

References

1). Neutrophil extracellular traps promote macrophage inflammation in psoriasis. Clinical Immunology, 2024 [IF=8.6]
2). Neutrophil extracellular traps induce a hypercoagulable state in glioma. Immunity Inflammation and Disease, 2021 (PubMed: 34288521) [IF=3.2]

Application: IF/ICC    Species: Human    Sample: glioma tissues

FIGURE 2 Platelet‐neutrophil interaction triggers NET generation in glioma patients. (A) Control neutrophils were incubated with PLT‐rich plasma from glioma patients and healthy subjects and stained with MPO (red) and DAPI (blue). (B) Plasma from stage III/IV glioma patients activated neutrophils to release higher proportions of NETs than those from stage I/II glioma patients and healthy subjects. (C) Immunofluorescence images also showed PLTs (CD41, green) decorated on DNA traps (DAPI, blue) when neutrophils (CD66b, red) were incubated with plasma from glioblastoma (GBM; stage IV glioma) patients. (D) PLT‐neutrophil aggregates, defined as CD41+/CD66b+ cells, were investigated in samples from each group. (E) The rate of PLT‐neutrophil aggregates was highest in samples from GBM patients. (F) Control neutrophils were incubated with PLTs from glioma patients and healthy subjects and analyzed by immunofluorescence microscopy. PLTs from stage III/IV glioma patients, especially GBM patients, were potent activators of NET formation than those from stage I/II glioma patients and healthy subjects. (G, H) Anti‐P‐selectin and PSGL‐1 antibodies were used to inhibit the interaction between neutrophils and PLTs and the NET (propidium iodide, red) formation was markedly decreased. The scale bar in (A) and (G) is 20 μm and (C) is 80μm. The results are expressed as the mean±SD. *p<.05, **p<.01, ***p<.001, and ****p<.0001. DAPI, 4′,6‐diamidino‐2‐ phenylindole; MPO, myeloperoxidase; NET, neutrophil extracellular trap; PLT, platelet

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