Module number 2727




Database revision : gnsdb28.10
Date : Tue Feb 25 17:27:43 2003
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mSRP1:karyopherin alpha homolog of 60 kDa,karyopherin alpha,supres\nsor of rpb1, cold-sensitive\n mRPT5:Probable 26S protease subunit and member of the CDC48/PAS1/S\nEC18 family of ATPases,,Null mutant is inviable\n mNEO1:ATPase that leads to neomycin-resistant protein when overexp\nressed,P-type ATPase,Null mutant is inviable. When overexpre\nssed, Neo1 confers neomycin resistance.\n mMOR1:Unknown ,, Unknown\n Jelinski.Jelinski:Regulatory networks revealed by transcriptional profiling of\n damaged Saccharomyces cerevisiae cells: Rpn4 links base exc\nision repair with proteasomes. Mol Cell Biol. 2000 Nov;20(2\n1):8157-67.\n mNAS6:Interaction with the 19S regulatory particle of the 26S prot\neasome detected by coimmunoprecipitation.,26S proteasome int\neracting protein,Null mutant is viable.\n mMRPS18:Unknown ,, Unknown\n mSNX4:Sorting NeXin,,\n Cond887:t-BuOOH\n mMRP49:16 kDa mitochondrial ribosomal large subunit protein,16 kDa \nmitochondrial ribosomal large subunit protein,Null mutant is\n viable, cold-sensitive, respiration deficient, defective in\n assembly of stable 54S ribosomal subunits\n mMSG1:Unknown ,, Unknown\n mSYS1:Multicopy suppressor of ypt6 null mutation,,Null mutant is v\niable. sys1 ypt6 double mutant displays enhanced defects in \nvacuolar sorting and cell growth\n Cond892:S\n mERG8:Involved in isoprene and ergosterol biosynthesis pathways,48\n kDa phosphomevalonate kinase,Null mutant is inviable\n Cond890:G1\n mGSH1:Glutathione biosynthesis,gamma-glutamylcysteine synthetase,N\null mutant is viable, exhibits alteration of glutathione con\ntent and reduction in growth rate\n mYIL135C:Unknown ,, Unknown\n Cond889:4NQO_2\n mSNF8:appears to be functionally related to SNF7,,Null mutant is v\niable, sporulation defective, grows poorly on raffinose as a\n carbon source, shows a five-fold decrease in invertase dere\npression\n mNMD4:putative Upf1p-interacting protein,,\n mYDR003W:Unknown ,, Unknown\n mPNP1:purine nucleoside phosphorylase, specifically metabolizes in\nosine and guanosine nucleosides,purine nucleoside phosphoryl\nase,null mutants excrete inosine and guanosine into the grow\nth medium\n mYMR115W:Unknown ,, Unknown\n mNPR1:protein kinase homolog,protein kinase homolog,inactive ammon\nia-sensitive amino acid permeases\n Cond873:10min\n Cond888:MNNG_2\n Cond894:G2\n mYMR221C:Unknown ,, Unknown\n mANT1:adenine nucleotide transporter,,Null: growth defect on mediu\nm-chain length fatty acids.\n mYHR162W:Unknown ,, Unknown\n mABF2:HMG-1 homolog, mitochondrial,HMG-1 homolog,\n mVID27:Vacuole import and degradation,,Null mutant is viable but ex\nhibits vacuole degradation of cytosolic proteins\n mYPR147C:Unknown ,, Unknown\n mPHO2:Regulation of phosphate metabolism,homeobox transcription fa\nctor , positive regulator of PHO5 and other genes , homeobox\n transcription factor , positive regulator of PHO5 and other\n genes,The null mutant is viable but unable to sporulate. Ma\nny genes regulated by GRF10 are expressed at non-wild type l\nevels in GRF10 null mutants.\n mYDR330W:Unknown ,, Unknown\n mERV41:ER vesicle protein,,Null mutant is viable.\n mYHR199C:Unknown ,, Unknown\n mDCP2:Mrna Decapping. essential suppressor of the respiratory defi\nciency of a pet mutant,,\n mULA1:Required for activation of RUB1 (ubiquitin-like protein) tog\nether with UBA3. Related to AOS1 and to N-terminus of UBA1. \nCollaborates with UBC12 in conjugation of RUB1 to other prot\neins. Required for modification of CDC53/cullin with RUB1,,N\null mutant is viable with no obvious mutant phenotype, is sy\nnthetically lethal with cdc34(ubc3) ts mutant, and enhances \nthe phenotypes of cdc4, cdc53, and skp1 mutants\n mRPN8:Regulatory Particle Non-ATPase, homolog of mammalian proteas\nomal subunit S12/p40,proteasome regulatory particle subunit,\n mAIP1:Protein localizes to actin cortical patches. Probable bindin\ng site on actin lies on front surface of subdomain 3 and 4.,\nactin cortical patch component,Null mutant is viable\n mNAB2:nuclear polyadenylated RNA binding protein,polyadenylated RN\nA binding protein,Null mutant is inviable\n mDPP1:contains a novel phosphatase sequence motif found in a super\n family of phosphatases including mammalian PAP2,diacylglyce\nrol pyrophosphate phosphatase,Null mutant is viable, does no\nt exhibit any obvious growth defects\n mNMA2:Unknown ,, Unknown\n mYKR070W:Unknown ,, Unknown\n mLYS5:aminoadipate-semialdehyde dehydrogenase small subunit (alpha\n-aminoadipate reductase),aminoadipate-semialdehyde dehydroge\nnase small subunit (alpha-aminoadipate reductase),Lysine req\nuiring\n mYPR172W:Unknown ,, Unknown\n mSTP3:Involved in pre-tRNA splicing and in uptake of branched-chai\nn amino acids,,\n Cond878:MNNG\n mSEC11:signal peptidase subunit,,Null mutant is inviable\n Cond879:MMC\n mYNR040W:Unknown ,, Unknown\n mUFD2:Ubiquitin fusion degradation protein,,Null mutant is viable \nbut exhibits increased sensitivity to ethanol stress.\n mLSC1:alpha subunit of succinyl-CoA ligase (synthetase; ATP-formin\ng), a mitochondrial enzyme of the TCA cycle,,Null mutant is \nviable but grows slowly on minimal glycerol or pyruvate; mut\nant suppresses idh2 null mutants for growth on glycerol\n mSEC15:Protein involved in vesicle traffic between Golgi and plasma\n membrane. The Exocyst complex is required for exocytosis.,e\nxocyst complex 113kDa component,The sec15-1 allele exhibits \ntemperature-sensitive growth and defects in the secretory pa\nthway.\n Cond882:zero3\n Cond877:MMS\n Cond875:60min\n mYNL063W:Unknown ,, Unknown\n mAPS2:Related to the sigma subunit of the mammalian plasma membran\ne clathrin-associated protein (AP-2) complex,clathrin associ\nated protein complex small subunit,null mutant is viable; sl\night effect on chc1-ts cell growth\n SGD.GO:Functional classification via a compendium of knockouts. Hug\nes et.al., cell 2000.\n mABZ1:para-aminobenzoate synthase, PABA synthase,para-aminobenzoat\ne synthase (PABA synthase),Null mutant is viable and PABA au\nxotroph\n mGLO1:Regulated by HOG (high osmolarity glycerol)-MAP (mitogen-act\nivated protein) kinase pathway in osmotic stress response,la\nctoylglutathione lyase (glyoxalase I),Null mutant is viable;\n sensitive to methylglyoxal\n mYNL115C:Unknown ,, Unknown\n mUBP6:deubiquitinating enzyme (putative),,\n mYPR021C:Unknown ,, Unknown\n mYDR107C:Unknown ,, Unknown\n mOST6:Putative new 37kDa subunit of N-oligosaccharyltransferase co\nmplex,N-oligosaccharyltransferase complex 37kDa subunit (put\native),\n Cond876:zero2\n mTAF6:TATA-binding protein-associated-factor,TATA-binding protein-\nassociated-factor,Null mutant is inviable\n Cond885:20\n mYTA7:Member of CDC48/PAS1/SEC18 family of ATPases,,\n mPCP1:Unknown ,, Unknown\n mTFC3:transcription factor tau (TFIIIC) subunit 138,138 kDa , tran\nscription factor tau (TFIIIC) subunit , 138 kDa , transcript\nion factor tau (TFIIIC) subunit,Null mutant is inviable\n mYHR113W:Unknown ,, Unknown\n mLTP1:Homologous to mammalian phosphotyrosine phosphatase,18 kDa p\nhosphotyrosine phosphatase,Null mutant is viable\n mSHR5:Involved in RAS localization and palmitoylation,,Null mutant\n is viable; exhibits normal palmityltransferase activity in \nvitro and attenuates Ras function in cells with mutant Ras2 \nproteins that are not farnesylated or palmitoylated; shr5 mu\ntation originally isolated as suppressor of Ras function\n mAPL2:Beta-adaptin, large subunit of the clathrin-associated prote\nin (AP-1) complex,beta-adaptin , clathrin associated protein\n complex large subunit,null mutant is viable\n mYMR298W:Unknown ,, Unknown\n mYJL072C:Unknown ,, Unknown\n Cond881:4NQO\n mMCK1:Disp. for mitosis, required for chr. segregation, benomyl re\nsist., basal IME1 transcript. in mitosis, IME1 induction in \nmeiosis & ascus mat. independ. of IME1; maybe in mitotic chr\n. segregation specific to CDEIII,43.1 kDa serine/threonine/t\nyrosine protein kinase,Null mutant is viable, cold sensitive\n, temperature sensitive, and benomyl sensitive; associated w\nith delays and decreased levels of sporulation. High copy MC\nK1 acclerates early gene expression.\n mKEM1:Kar1-1 nuclear-fusion-defect Enhancing Mutation. Plays a rol\ne in cytoplasmic mRNA degradation.,5'-3' exonuclease,Null mu\ntant is viable but grows poorly. kem1 mutants exhibit aberra\nnt mRNA turnover and are are thought to be very pleiotropic \nas a result; elongated morphology, defective in spindle-pole\n-body duplication/separation and telomere maintenance, benom\nyl hypersensitive, 10-20-fold elevation in chromosome loss, \ndecreased mitotic recombination and inviable upon nitrogen s\ntarvation includes a partial list of phenotypes.\n mYKR065C:Unknown ,, Unknown\n mNTA1:Removes amide group from N-terminal asparagine and glutamine\n, to generate aspartate and glutamate, which are destabilizi\nng terminal residues,52 kDa amidase specific for N-terminal \nasparagine and glutamine,Null mutant is viable but cannot de\ngrade N-end rule substrates that have N-terminal asparagine \nor glutamine\n mUGT51:Udp-glycosyltransferase,UDP-glucose:sterol glucosyltransfera\nse,Null mutant is viable and unable to synthesize sterol glu\ncoside\n mERV25:COPII coat component of certain ER-derived vesicles,vesicle \ncoat component,Null mutant is viable, displays a selective d\nefect in transport of secretory proteins from the ER to Golg\ni complex.\n mYGR011W:Unknown ,, Unknown\n mYLR454W:Unknown ,, Unknown\n mPRC1:dispensable for haploidization and sporulation, but required\n for full protein degradation during sporulation,carboxypept\nidase Y (proteinase C),Null mutant is viable,proteinase C de\nficient\n mSGN1:contains one RNA recognition (RRM) domain,,\n mERV29:ER Vesicle protein of 29 kDa (apparent MW),ER-Golgi transpor\nt vesicle protein,Null mutant is viable.\n mYOL098C:Unknown ,, Unknown\n mBET2:Geranylgeranyltransferase Type II beta subunit,geranylgerany\nltransferase type II beta subunit,Null mutant is inviable\n mBET3:Hydrophilic protein that acts in conjunction with SNARE prot\neins in targeting and fusion of ER to Golgi transport vesicl\nes,transport protein particle (TRAPP) component,Null mutant \nis inviable\n mLCB5:involved in sphingolipid biosynthesis,sphingoid long chain b\nase (LCB) kinase,Null mutant is viable, exhibits approximate\nly 97% of wild-type LCB kinase activity; lcb4 lcb5 double de\nletion mutants exhibit no LCB kinase activity\n Cond884:10\n mHST1:Homolog of SIR2,,Overexpression restores transcriptional sil\nencing in a sir2 mutant\n
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Computational Genomics Lab, Tel-Aviv uniresity