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AB110825

Anti-CEP152 antibody

0

(1 Review)

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(1 Publication)

Rabbit Polyclonal CEP152 antibody. Suitable for IHC-P and reacts with Human samples. Cited in 1 publication. Immunogen corresponding to Synthetic Peptide within Human CEP152.

View Alternative Names

KIAA0912, CEP152, Centrosomal protein of 152 kDa, Cep152

1 Images
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-CEP152 antibody (AB110825)
  • IHC-P

Unknown

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-CEP152 antibody (AB110825)

ab110825, at 1/50 dilution, staining CEP152 in paraffin-embedded Human lymph node tissue by Immunohistochemistry, in the presence (right panel) or absence (left panel) of immunising peptide.

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

IHC-P

applications

Immunogen

Synthetic Peptide within Human CEP152. The exact immunogen used to generate this antibody is proprietary information.

O94986

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "IHCP" : {"fullname" : "Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections)", "shortname":"IHC-P"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Human": { "IHCP-species-checked": "testedAndGuaranteed", "IHCP-species-dilution-info": "1/50 - 1/100", "IHCP-species-notes": "<p></p> Perform heat-mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol." } } }

Properties and storage information

Form
Liquid
Purification technique
Affinity purification Immunogen
Purification notes
ab110825 was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Storage buffer
pH: 7.4 Preservative: 0.02% Sodium azide Constituents: PBS, 50% Glycerol (glycerin, glycerine), 0.88% Sodium chloride
Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Storage information
Stable for 12 months at -20°C

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

CEP152 also known as centrosomal protein of 152 kDa is a component of the centrosome and plays a critical mechanical role in cell division. It weighs approximately 152 kilodaltons and is expressed in various tissues primarily during the cell cycle. CEP152 functions as a scaffold protein aiding in the recruitment and organization of other proteins involved in centrosome-related processes. These activities make it an essential player in maintaining centrosome integrity and ensuring the correct duplication of centrioles which are pivotal for proper spindle formation and chromosome segregation.
Biological function summary

The protein plays a significant role in the regulation of genomic stability and cell cycle progression. It forms part of a complex with other centrosomal proteins such as CEP63 which further enhances its role in centrosome duplication. This cooperation between proteins ensures that cells properly manage centrosome replication and prevent abnormalities that could lead to genomic instability. CEP152 also interacts with kinases to modulate centrosomal activities and help maintain genetic fidelity during cell division.

Pathways

CEP152 integrates into the centrosome cycle and DNA damage response pathways. The protein actively participates in centrosome assembly working in conjunction with proteins like CEP192 to control centriole duplication and maturation. Additionally CEP152 influences the ATR signaling pathway which is a critical pathway for responding to DNA damage and maintaining cell cycle checkpoints. Through these interactions CEP152 helps synchronize cell cycle events with DNA repair processes therefore ensuring cellular homeostasis.

CEP152 links to microcephalic primordial dwarfism and certain cancers. Mutations in CEP152 can lead to reduced brain size and associated developmental disorders connecting it with the disease condition microcephalic osteodysplastic primordial dwarfism type I (MOPD I). In cancer altered expressions of CEP152 have been implicated in tumorigenesis often due to its association with the misregulation of cell cycle pathways. The protein's connection to PLK4 a pivotal regulator of centriole duplication highlights its importance in maintaining centrosomal functions and its potential role in cancer when these processes go awry.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

Necessary for centrosome duplication; the function seems also to involve CEP63, CDK5RAP2 and WDR62 through a stepwise assembled complex at the centrosome that recruits CDK2 required for centriole duplication (PubMed : 26297806). Acts as a molecular scaffold facilitating the interaction of PLK4 and CENPJ, 2 molecules involved in centriole formation (PubMed : 20852615, PubMed : 21059844). Proposed to snatch PLK4 away from PLK4 : CEP92 complexes in early G1 daughter centriole and to reposition PLK4 at the outer boundary of a newly forming CEP152 ring structure (PubMed : 24997597). Also plays a key role in deuterosome-mediated centriole amplification in multiciliated that can generate more than 100 centrioles (By similarity). Overexpression of CEP152 can drive amplification of centrioles (PubMed : 20852615).
See full target information CEP152

Publications (1)

Recent publications for all applications. Explore the full list and refine your search

Oncology research 28:299-309 PubMed31969212

2020

MafF Is Regulated via the circ-ITCH/miR-224-5p Axis and Acts as a Tumor Suppressor in Hepatocellular Carcinoma.

Applications

Unspecified application

Species

Unspecified reactive species

Minhua Wu,Xubin Deng,Yu Zhong,Li Hu,Xiujuan Zhang,Yanqin Liang,Xiaofang Li,Xiaoxia Ye
View all publications

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