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MEC1 Mec1p

Mec1, Mec1p, mecI
The protein encoded by this gene belongs the PI3/PI4-kinase family, and is most closely related to ATM, a protein kinase encoded by the gene mutated in ataxia telangiectasia. This protein and ATM share similarity with Schizosaccharomyces pombe rad3, a cell cycle checkpoint gene required for cell cycle arrest and DNA damage repair in response to DNA damage. This kinase has been shown to phosphorylate checkpoint kinase CHK1, checkpoint proteins RAD17, and RAD9, as well as tumor suppressor protein BRCA1. Mutations of this gene are associated with Seckel syndrome. An alternatively spliced transcript variant of this gene has been reported, however, its full length nature is not known. Transcript variants utilizing alternative polyA sites exist. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Chk2, Atm, Rad9, CAN, Rad17
Papers on Mec1
Gene network analysis reveals the association of important functional partners involved in antibiotic resistance: A report on an important pathogenic bacterium Staphylococcus aureus.
Ramaiah et al., Vellore, India. In Gene, Feb 2016
We filtered 50 functional partners in NorA, aacA-aphD (aac6ie), aad9ib (ant), aadd (knt), baca (uppP), bl2a_pc (blaZ), ble, ermA, SAV0052 (ermb), ermc, fosB, mecA (mecI), mecR (mecr1), mepA, msrA1, qacA, vraR (str), tet38 and tetM while 40 functional partners are identified in tet and aphA-3 (aph3iiia).
Wnt5a induces ROR1/ROR2 heterooligomerization to enhance leukemia chemotaxis and proliferation.
Kipps et al., In J Clin Invest, Jan 2016
Using the ROR1-deficient CLL cell line MEC1, we demonstrated that ectopic ROR1 expression induced ROR1/ROR2 heterooligomers, which recruited GEFs, and enhanced proliferation, cytokine-directed migration, and engraftment potential of MEC1 cells in immune-deficient mice.
Whole-genome analysis of an oxacillin-susceptible CC80 mecA-positive Staphylococcus aureus clinical isolate: insights into the mechanisms of cryptic methicillin resistance.
Friedrich et al., Groningen, Netherlands. In J Antimicrob Chemother, Nov 2015
GR2 carried SCCmec type IV, with a truncated/non-functional mecR1 gene and no mecI.
Checkpoint Activation of an Unconventional DNA Replication Program in Tetrahymena.
Kapler et al., College Station, United States. In Plos Genet, Jul 2015
The intra-S phase checkpoint kinase of metazoa and yeast, ATR/MEC1, protects chromosomes from DNA damage and replication stress by phosphorylating subunits of the replicative helicase, MCM2-7.
Mechanisms of Methicillin Resistance in Staphylococcus aureus.
Paterson et al., Cambridge, United Kingdom. In Annu Rev Biochem, 2014
PBP2a is encoded by the mecA gene, which is carried on a distinct mobile genetic element (SCCmec), the expression of which is controlled through a proteolytic signal transduction pathway comprising a sensor protein (MecR1) and a repressor (MecI).
S phase block following MEC1ATR inactivation occurs without severe dNTP depletion.
Cha et al., Umeå, Sweden. In Biol Open, 2014
Inactivation of Mec1, the budding yeast ATR, results in a permanent S phase arrest followed by chromosome breakage and cell death during G2/M.
Antimicrobial Effects and Resistant Regulation of Magnolol and Honokiol on Methicillin-Resistant Staphylococcus aureus.
Yu et al., Chŏnju, South Korea. In Biomed Res Int, 2014
Furthermore, the magnolol inhibited the expression of the resistant genes, mecA, mecI, femA, and femB, in mRNA.
Key genetic elements and regulation systems in methicillin-resistant Staphylococcus aureus.
Yuan et al., Wuhan, China. In Future Microbiol, 2012
S. aureus has developed methicillin resistance mainly by expression of β-lactamase and PBP2a, which is regulated by the blaZ-blaI-blaR1 and mecA-mecI-mecRI systems.
ATM/ATR checkpoint activation downregulates CDC25C to prevent mitotic entry with uncapped telomeres.
Tarsounas et al., Oxford, United Kingdom. In Embo J, 2012
Dysfunctional telomeres promote ATM/ATR-dependent degradation of CDC25C phosphatase to block mitotic entry, thereby preventing telomere dysfunction-driven genomic instability.
Targeting radiation-resistant hypoxic tumour cells through ATR inhibition.
Hammond et al., Oxford, United Kingdom. In Br J Cancer, 2012
VE-821 was shown to inhibit ATR-mediated signalling in response to replication arrest induced by severe hypoxia.
ATP depletion triggers acute myeloid leukemia differentiation through an ATR/Chk1 protein-dependent and p53 protein-independent pathway.
Wald et al., Cleveland, United States. In J Biol Chem, 2012
Data indicate that acute myeloid leukemia differentiation can be induced through ATP depletion and the subsequent activation of DNA damage signaling through an ATR/Chk1-dependent and p53-independent pathway.
Hypoxia activates tumor suppressor p53 by inducing ATR-Chk1 kinase cascade-mediated phosphorylation and consequent 14-3-3γ inactivation of MDMX protein.
Lu et al., Indianapolis, United States. In J Biol Chem, 2012
hypoxia can activate p53 through inactivation of MDMX by the ATR-Chk1-MDMX-14-3-3gamma pathway.
Meiotic DNA double-strand breaks and chromosome asynapsis in mice are monitored by distinct HORMAD2-independent and -dependent mechanisms.
Tóth et al., Dresden, Germany. In Genes Dev, 2012
these observations strongly suggest that HORMAD2-dependent recruitment of ATR to unsynapsed chromosome axes constitutes a mechanism for the surveillance of asynapsis.
DNA damage signalling prevents deleterious telomere addition at DNA breaks.
Blackburn et al., San Francisco, United States. In Nat Cell Biol, 2009
Using yeast, we show that the main ATR/Mec1 DNA damage signalling pathway regulates telomerase action at DSBs.
A two-step model for senescence triggered by a single critically short telomere.
Teixeira et al., Lyon, France. In Nat Cell Biol, 2009
Data suggest that in the absence of telomerase, a very short telomere is first maintained in a pre-signalling state by a RAD52-MMS1-dependent pathway and then switches to a signalling state leading to senescence through a Mec1p-dependent checkpoint.
Impaired tRNA nuclear export links DNA damage and cell-cycle checkpoint.
Emili et al., Toronto, Canada. In Cell, 2007
This response requires an intact MEC1- and RAD53-dependent signaling pathway that impedes the nuclear export of intron-containing tRNA via differential relocalization of the karyopherin Los1 to the cytoplasm.
Role of the error-free damage bypass postreplication repair pathway in the maintenance of genomic stability.
Klein et al., New York City, United States. In Mutat Res, 2003
The DNA damage checkpoint gene MEC1 acts synergistically with the PRR pathway in maintaining genomic stability.
A Rad53 kinase-dependent surveillance mechanism that regulates histone protein levels in S. cerevisiae.
Verreault et al., London, United Kingdom. In Cell, 2003
Rad53 and Mec1 are protein kinases required for DNA replication and recovery from DNA damage in Saccharomyces cerevisiae.
Methicillin-resistant Staphylococcus aureus. Mechanisms of resistance and implications for treatment.
Chambers, San Francisco, United States. In Postgrad Med, 2001
Two genes located upstream from mecA--mecR1 and mecI--control expression of PBP-2a.
Examining the Distribution of Telomeric and DNA Repair Proteins by ChrIP and Real-Time PCR
Dubrana, Paris, France. In Unknown Journal, 0001
The Mec1 protein itself associates with DSB in a yKu-independent manner but does not localize to telomeres, even in the presence of DNA damage, suggesting that Mec1p may act indirectly on telomeric proteins.
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