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anti-Mouse (Murine) CEP164 Antikörper:
anti-Rat (Rattus) CEP164 Antikörper:
anti-Human CEP164 Antikörper:
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Human Polyclonal CEP164 Primary Antibody für ICC, IF - ABIN4297726
Schueler, Braun, Chandrasekar, Gee, Klasson, Halbritter, Bieder, Porath, Airik, Zhou, LoTurco, Che, Otto, Böckenhauer, Sebire, Honzik, Harris, Koon, Gunay-Aygun, Saunier, Zerres, Bruechle, Drenth et al.: DCDC2 mutations cause a renal-hepatic ciliopathy by disrupting Wnt signaling. ... in American journal of human genetics 2015
Show all 7 Pubmed References
Studies unravel unique requirements for CEP164 in primary versus multiciliogenesis and suggest that CEP164 modulates the selective transport of membrane vesicles and their cargoes into the ciliary compartment in multiciliated cells.
data suggest that CEP164 is not required in the DNA damage response.
This study reveals a novel role for CEP164 in the pathogenesis of nephronophthisis, in which mutations cause ciliary defects coupled with DNA damage induced replicative stress, cell death, and epithelial-to-mesenchymal transition
Evidence is provided that TTBK2 effectively phosphorylate Cep164 and Cep97 and inhibits the interaction between Cep164 and its binding partner Dishevelled-3 (an important regulator of ciliogenesis) in a kinase activity-dependent manner.
data suggest that TTBK2 also acts upstream of Cep164, contributing to the assembly of distal appendages
Cep164 is targeted to the apical domain of the mother centriole to provide the molecular link between the mother centriole and the membrane biogenesis machinery that initiates cilia formation.
findings indicate that ARL13B, INPP5E, PDE6D, and CEP164 form a distinct functional network that is involved in JBTS and NPHP but independent of the ones previously defined by NPHP and MKS proteins
Study identifies by whole-exome resequencing, mutations of MRE11, ZNF423, and CEP164 as causing Nephronophthisis-related ciliopathies.
Single nucleotide polymorphisms of CCND2, RAD23B, GRP78, CEP164, MDM2, and ALDH2 genes were significantly associated with development and recurrence of hepatocellular carcinoma in Japanese patients with hepatitis C virus.
These data implicate distal appendages in primary cilia formation and identify Cep164 as an excellent marker for these structures.
Cep164 is a key player in the DNA damage-activated signaling cascade.
Results show that Cep164 knockdown compromises the cell survival upon UV damage, and that UV irradiation significantly enhances the interaction between Cep164 and XPA.
This gene encodes a centrosomal protein involved in microtubule organization, DNA damage response, and chromosome segregation. The encoded protein is required for assembly of primary cilia and localizes to mature centrioles. Defects in this gene are a cause of nephronophthisis-related ciliopathies. Two transcript variants encoding different isoforms have been found for this gene.
centrosomal protein 164kDa
, centrosomal protein of 164 kDa-like
, centrosomal protein of 164 kDa