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MAD1 and Proto-Oncogene Proteins c-myc reciprocally regulate ribosomal DNA transcription, providing a mechanism for coordination of ribosome biogenesis and cell growth
MAD1 is present in mouse oocytes at all stages during the first meiosis and that it participates in spindle checkpoint during meiosis
Data show that the loss of Trrap leads to chromosome missegregation, mitotic exit failure and compromised mitotic checkpoints, which are caused by defective Trrap-mediated transcription of the mitotic checkpoint proteins Mad1 and Mad2.
identified mouse Telomeric Repeat Binding Factor 1 (Trf1) as a protein that interacts directly with the spindle checkpoint protein Mad1 and the mitotic kinase Nek2
Together these data demonstrate that the MYC-antagonist MAD1 and cyclin-dependent kinase inhibitor p27(Kip1) cooperate to regulate the self-renewal and differentiation of HSCs in a context-dependent manner.
the simultaneous knockdown of p18, p27 and MAD1 with a medium of only stem cell factor can induce long-term culture-initiating cell expansion despite the loss of engraftment ability
Data suggest that LMO7 interacts with MAD1 during spindle assembly phase of mitosis; LMO7 plays role in control of mitosis progression and exerts effect on spindle assembly checkpoint; LMO7 colocalizes with actin filaments; LMO7 does not colocalize with MAD1 at kinetochores in prometaphase nor at spindle poles in metaphase. (LMO7 = LIM domain only protein-7; MAD1 = mitotic spindle assembly checkpoint protein MAD1)
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.
This study showed that MAD1L1 as a susceptibility gene for both of these genetically overlapping disorders is associated with a decreased bottom-up responsiveness of the mesolimbic reward system and related cortical regions involved in the salience network as well as with reduced top-down control processes.
Results show that low DNA methylation levels of LINC00682, MAD1L1, and LINE-2 was strongly correlated with hepatocellular carcinomas recurrence, patient disease-free survival, and/or overall survival.
MAD1L1 positive expression may be associated with tumour progression and metastasis in small-cell lung cancer (SCLC) and may thus serve as a new biomarker for prognosis in these patients.
In this review, we highlight a novel Mad1 role in chromosome alignment, which is the first conserved mechanism that links the spindle assembly checkpoint and kinesin-mediated chromosome gliding.
MAD1L1 Arg558His and MAD2L1 Leu84Met interaction with smoking increase the risk of colorectal cancer
MAD1L1 rs12666575 polymorphism may play a protective role against schizophrenia (SCZ) in the Chinese population. rs12666575 may be associated with general psychopathology and thought disturbance in SCZ patients.
We also show that replication perturbations result in relocalization of MAD1/MAD2 in human cells, suggesting that the role of SAC in DNA repair is conserved.
Mad1 has a role in secretion and cell migration.
MAD1 kinetochore localization dictates the spindle assembly checkpoint in metaphase.
This article reviews Mad1 and Mad2 - structural and functional relationship with implication in genetic diseases, specifically in cancer. [review]
Mad1 is required for mitotic arrest even when C-Mad2 is artificially recruited to kinetochores. The C-terminal globular domain of Mad1 and conserved residues in this region are required for this unexpected function of Mad1.
An important role of ATM-mediated Mad1 Serine 214 phosphorylation in mitosis.
Here we demonstrate that the centromere protein CENP-I is required to generate a stable association of RZZ and Mad1 with kinetochores.
PRAP1 is a protein interacting partner of MAD1 and that PRAP1 is able to down-regulate MAD1 and suppress mitotic checkpoint signalling in hepatocellular carcinoma.
Mad1, in addition to converting Mad2 to its active conformation, scaffolds formation of a higher-order mitotic checkpoint complex at kinetochores.
Results show that Mad1-Mad2 must be targeted to nuclear pore complexes (NPCs) in order to produce the premitotic Cdc20 inhibitor, which ensures that anaphase and mitotic exit are robustly coupled to the establishment and correction of kinetochore-microtubule attachments.
Tpr is required for normal SAC response by stabilizing Mad1 and Mad2 before mitosis.
MAD1L1 might be used as a prognostic biomarker for breast cancer and expression of MAD1L1 in nuclei is also a predict biomarker of contraindication to pacilitaxel treatment in breast cancer.
MAD1L1 is a component of the mitotic spindle-assembly checkpoint that prevents the onset of anaphase until all chromosome are properly aligned at the metaphase plate. MAD1L1 functions as a homodimer and interacts with MAD2L1. MAD1L1 may play a role in cell cycle control and tumor suppression. Three transcript variants encoding the same protein have been found for this gene.
MAD1-like protein 1
, mitotic arrest deficient 1-like 1
, mitotic arrest deficient 1-like protein 1
, mitotic spindle assembly checkpoint protein MAD1
, mitotic checkpoint MAD1 protein homolog
, mitotic-arrest deficient 1, yeast, homolog-like 1
, tax-binding protein 181
, tumor protein p53 inducible protein 9