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Rabbit Anti-CEP152/APC Conjugated antibody
Rabbit Anti-CEP152/APC Conjugated antibody
CE152_HUMAN; Centrosomal protein 152kDa; Centrosomal protein of 152 kDa; Cep152; FLJ21594; KIAA0912; MCPH4.
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  • NO.:SL7787R-APC
    Clonality:Polyclonal
    Immunogen Species:Rabbit
    React Species:(predicted: Human,Mouse,Rat,Dog,Horse,)
    Applications:IF
    concentration:1mg/ml
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Product Name Anti-CEP152/APC
Chinese Name APC标记的中心体蛋白152抗体
Alias CE152_HUMAN; Centrosomal protein 152kDa; Centrosomal protein of 152 kDa; Cep152; FLJ21594; KIAA0912; MCPH4.  
Research Area Cell biology  Cyclin  Cell differentiation  Epigenetics  
Immunogen Species Rabbit
Clonality Polyclonal
React Species (predicted: Human, Mouse, Rat, Dog, Horse, )
Applications IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
Molecular weight 189kDa
Form Lyophilized or Liquid
Concentration 1mg/ml
immunogen KLH conjugated synthetic peptide derived from human CEP152
Lsotype IgG
Purification affinity purified by Protein A
Storage Buffer 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage 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.
Product Detail background:
Defects in CEP152 are the cause of microcephaly primary type 4 (MCPH4). A disease defined as a head circumference more than 3 standard deviations below the age-related mean. Brain weight is markedly reduced and the cerebral cortex is disproportionately small. Despite this marked reduction in size, the gyral pattern is relatively well preserved, with no major abnormality in cortical architecture. Affected individuals are mentally retarded. Primary microcephaly is further defined by the absence of other syndromic features or significant neurological deficits due to degenerative brain disorder.

Function:
Regulator of genomic integrity and cellular response to DNA damage acting through ATR-mediated checkpoint signaling. Necessary for centrosome duplication. It functions as a molecular scaffold facilitating the interaction of PLK4 and CENPJ, two molecules involved in centriole formation.

Subunit:
Interacts (via N-terminus) with PLK4. Interacts (via C-terminus) with CENPJ (via-N-terminus). Interacts with CINP. Interacts with CEP63; this interaction recruits CEP152 to centrosomes.

Subcellular Location:
Cytoplasm, cytoskeleton, centrosome. Note=Colocalizes with CEP63 in a discrete ring around the proximal end of the parental centriole. At this site, a cohesive structure is predicted to engage parental centrioles and procentrioles.

DISEASE:
Defects in CEP152 are the cause of microcephaly primary type 4 (MCPH4) [MIM:604321]. A disease defined as a head circumference more than 3 standard deviations below the age-related mean. Brain weight is markedly reduced and the cerebral cortex is disproportionately small. Despite this marked reduction in size, the gyral pattern is relatively well preserved, with no major abnormality in cortical architecture. Affected individuals are mentally retarded. Primary microcephaly is further defined by the absence of other syndromic features or significant neurological deficits due to degenerative brain disorder.
Defects in CEP152 are the cause of Seckel syndrome type 5 (SCKL5) [MIM:613823]. A rare autosomal recessive disorder characterized by proportionate dwarfism of prenatal onset associated with low birth weight, growth retardation, severe microcephaly with a bird-headed like appearance, and mental retardation.

Database links:
UniProtKB/Swiss-Prot: O94986.3

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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