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anti-Human CASC5 Anticorps:
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Human Polyclonal CASC5 Primary Antibody pour ICC, IF - ABIN251026
Zhang, Zhang, Gao, Wang, Jin, Wei, Saiyin, Wang, Peng, Ma, Tang, Wumaier, Yu, Dong, Huang, Yu, Wang: ASPP1/2-PP1 complexes are required for chromosome segregation and kinetochore-microtubule attachments. dans Oncotarget 2015
Human Polyclonal CASC5 Primary Antibody pour ICC, IF - ABIN4287959
Milev, Hasaj, Saint-Dic, Snounou, Zhao, Sacher: TRAMM/TrappC12 plays a role in chromosome congression, kinetochore stability, and CENP-E recruitment. dans The Journal of cell biology 2015
Data show how KNL1 binds both PP1 and microtubules. Unexpectedly, PP1 and microtubules bind KNL1 via overlapping binding sites. Co-sedimentation assays unequivocally demonstrated that microtubules and PP1 binding to KNL1 is mutually exclusive, with preferential formation of the KNL1:PP1 holoenzyme in the presence of PP1.
Study demonstrates that KNL1 acts as a receptor of linear ubiquitin chains to anchor CENP-E at attached kinetochores. Thus, linear ubiquitin chains constitute a critical mechanism for chromosome congression and alignment by coupling the dynamic kinetochore microtubule motor CENP-E to the static one, the KMN network.
Mutations in the CASC5 gene were found to encode a kinetochore protein essential for mitotic cell division and to cause autosomal recessive primary microcephaly 4. (Review)
Therefore, Mps1 promotes checkpoint activation through sequentially phosphorylating Knl1, Bub1, and Mad1. This sequential multi-target phosphorylation cascade makes the checkpoint highly responsive to Mps1 and to kinetochore-microtubule attachment.
CASC5 may contribute to the morphological and structural changes of the human brain during recent evolution. The observed between-population divergence of CASC5 variants was driven by natural selection that tends to favor a larger gray matter volume in East Asians.
Involvement of CASC5 in autosomal recessive microcephaly and a founder effect of the c.6125G>A mutation.
Targeted Knockdown of the Kinetochore Protein D40/Knl-1 Inhibits Human Cancer in a p53 Status-Independent Manner
We propose that CASC5 has a key role for the correct functioning of DNA damage response proteins, and a defect in this connection might affect upstream and downstream DNA damage response events as response to increased genotoxic stress.
Data show sequential multisite regulation of the microtubule-associated protein KNL1-kinase-adaptor complex BUB1/BUB3 interaction.
Mechanisms of mitosis-specific assembly of the checkpoint platform Knl1/MIS12/NDC80 at human kinetochores.
PP2A-B56 is a key phosphatase for the removal of the Mps1-mediated Knl1 phosphorylations necessary for Bub1/BubR1 recruitment in mammalian cells.
Protein phosphatase 1 (PP1) binding to KNL1 during prometaphase reduces the levels of Bub proteins at kinetochores to approximately the level recruited by four active MELT repeats.
In cells depleted of endogenous Knl1, kinetochore-targeted Knl1(1-250) suffices to restore spindle assembly checkpoint and chromosome alignment
KNL1 contains an extensive array of short linear sequence modules that encompass TxxOmega and MELT motifs and that can independently localize BUB1.
KNL1 is a requirement for Aurora B activity at kinetochores and for wild-type kinetochore-MT attachment dynamics.
Data provide strong evidence for CASC5 as a novel MCPH gene, and underscore the role of kinetochore integrity in proper volumetric development of the human brain.
we identify the Blinkin motif critical for interaction with BUBR1, define the stoichiometry and affinity of the interaction, and present a 2.2 Angstrom resolution crystal structure of the complex
Expression levels of D40 mRNA and proteins decrease according to the degree of spermatogenesis impairment in male infertile patients.
h-KNL1 functions to connect Bub1 and BubR1 with the hMis12, Ndc80, and Zwint-1 complexes.
phosphorylation of KNL1 by Aurora B disrupts the KNL1-PP1 interaction
Study in mouse model finds that following Knl1 deletion, segregation errors in mitotic neural progenitor cells give rise to DNA damage on the missegregated chromosomes. This triggers rapid p53 activation and robust apoptotic and microglial phagocytic responses that extensively eliminate cells with somatic genome damage, thus causing microcephaly.
Data indicate that microtubule-associated proteins KNL-1 oligomerization may coordinate with other kinetochore activities to ensure the proper organization, function, and sensory capabilities of the kinetochore-microtubule attachment.
KNL-1 plays a central role in translating the initiation of kinetochore assembly
The protein encoded by this gene is a component of the multiprotein assembly that is required for creation of kinetochore-microtubule attachments and chromosome segregation. The encoded protein functions as a scaffold for proteins that influence the spindle assembly checkpoint during the eukaryotic cell cycle and it interacts with at least five different kinetochore proteins and two checkpoint kinases. In adults, this gene is predominantly expressed in normal testes, various cancer cell lines and primary tumors from other tissues and is ubiquitously expressed in fetal tissues. This gene was originally identified as a fusion partner with the mixed-lineage leukemia (MLL) gene in t(11\;15)(q23\;q14). Mutations in this gene cause autosomal recessive primary microcephaly-4 (MCPH4). Alternative splicing results in multiple transcript variants encoding different isoforms. Additional splice variants have been described but their biological validity has not been confirmed.
cancer susceptibility candidate 5
, ALL1-fused gene from chromosome 15q14 protein
, blinkin, bub-linking kinetochore protein
, cancer susceptibility candidate gene 5 protein
, cancer/testis antigen 29
, kinetochore null 1 homolog
, kinetochore-null protein 1
, protein CASC5
, protein phosphatase 1, regulatory subunit 55
, RAD51 homolog