What further experiments are needed to provide confidence that the structural data obtained from the SCAM analysis reflects the structure of a properly folded AlaE?
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What further experiments are needed to provide confidence that the structural data obtained from the SCAM analysis reflects the structure of a properly folded AlaE?
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- The full amino acid sequence of FABP6 is MAFTGKFEMECEKNYDEFMKLLGISSDVIEKARNFKIVTEVQQDGQDF TWSQHYSGGHTMTNKFTVGKECNIQTMGGKTFKATVQMEGGKLVVN FPNYHQTSEIVGDKLVEVSTIGGVTYERVSKRLA For the next step in your analysis, you ran a BLAST search of the PDB of this sequence and found a structure that is 59% identical to the sequence of your protein. The following is the alignment of two sequences (with your protein in blue (FABP6) and the homologous structure in red (3ELX)): Expect score = : 4 × 10−4² and Identities = 69/116(50%), Positives = 88/116(75%) 3ELX: 5 AFNGKWETECQEGYEPFCKLIGIPDDVIAKGRDFKLVTEIVQNGDDFTWTQYYPNNHVMT 64 AF GK + E EC++ Y+ F KL GI DVI K R+FK+VTE+ Q+G DFTW+Q+Y FABP6: 2 AFTGKFEMECEKNYDEFMKLLGISSDVIEKARNFKIVTEVQQDGQDFTWSQHYSGGHTMT 61 3ELX: 65 NKF IVGKECDMETVGGKKFKG IVSMEGGKLT IS FPKYQQTTEISGGKLVETSTASG 120 NKF VGKEC+++T+GGK FK V MEGGKL ++FP Y QT+EI G KLVE ST G FABP6: 62 NKFTVGKECNIQTMGGKTFKATVQMEGGKLVVNFPNYHQTSEIVGDKLVEVSTIGG H MT 117 The identical amino acids are shown in black…Sequence: CCACCTGTACCCGGACACACCCTGGTGTCC 1. Identify the gene from which the querysequence originates (Name of gene) 2. Provide the FULLprotein sequence encoded by the gene. 3. Are different splice variants known for this gene? 4. What human disease has been connected to this gene? 5. Calculate molecular weight (kiloDalton, kD) and calculated pI (the pH where the protein carries no net electrical charge) of the protein.Homozygosity for extremely rare mutations in a humangene called SCN9A cause complete insensitivity topain (congenital pain insensitivity or CPA) and a totallack of the sense of smell (anosmia). The SCN9A geneencodes a sodium channel protein required for transmission of electrical signals from particular nerves inthe body to the brain. The failure to feel pain is a dangerous condition as people cannot sense injuries.The SCN9A gene has 26 exons and encodes a1977-amino acid polypeptide. Consanguineous matings in three different families have resulted in individuals with CPA/anosmia. In Family 1, a G-to-Atransition in exon 15 results in a truncated protein that is898 amino acids long; in Family 2, deletion of a singlebase results in a 766-amino acid polypeptide; and inFamily 3, a C-to-G transversion in exon 10 yields a458-amino acid protein.a. Hypothesize as to how each of the three SCN9Amutations affects gene structure: Why are truncatedproteins made in each case? b. How would you…
- Low-resolution X-ray diffraction analysis of a protein composed of long stretches of the sequence (-Gly-Ser-Gly-Ala-Gly-Ala-)n, where n indicates any number of repeats, shows an extended structure of stacked layers, with a repeat distance between layers that alternates between 3.5 Å and 5.7 Å. Propose a model that explains this scenario.please help explain Influenza A virus M2 protein triggers mitochondrial DNA-mediated antiviral immune responses Cytosolic mitochondrial DNA (mtDNA) activates cGAS-mediated antiviral immune responses, but the mechanism by which RNA viruses stimulate mtDNA release remains unknown. Here we show that viroporin activity of influenza virus M2 or encephalomyocarditis virus (EMCV) 2B protein triggers translocation of mtDNA into the cytosol in a MAVS-dependent manner. Although influenza virus-induced cytosolic mtDNA stimulates cGAS- and DDX41- dependent innate immune responses, the nonstructural protein 1 (NS1) of influenza virus associates with mtDNA to evade the STING-dependent antiviral immunity. The STINGdependent antiviral signaling is amplified in neighboring cells through gap junctions. In addition, we find that STING-dependent recognition of influenza virus is essential for limiting virus replication in vivo. Our results show a mechanism by which influenza virus stimulates mtDNA release…The estimated size of fusion protein of an antibiotic (540bp) and an anti-inflammatory agent (630 bp). There are an additional 222 bp between the sequences. Assuming the average weight of an amino acid is 114 Da, what is the estimated size of the fusion protein? 53 kDa 44 kDa 59 kDa 159 kDa
- Beer's Law to determine Protein Concentration You have purified a recombinant form of the p53 protein from E. coli and determined the A280 to be1.35. Calculate the molar and mass concentration of the purified protein if the extinction coefficientand molecular weight of p53 is 35,410 M-1 cm-1 and 43,653 Da, respectively (l = 1 cm).QUESTION: Transcribe the gene. Write out the correct sequence of m RNA bases. Notice that this is the same gene as in B above. Recall that in RNA, thymine (T) does not exist and uracil (U) takes its place. 3' ССА TAG CÁC CTT GTC ACA ACG TGT TCG TAG ACA 1 3. 4. 6. 7. 8. 9- 10 11 AGG AAC АТА ATA GTT AAC CTT TTG ATA ACA ТТА ACT 12 13 14 15 16 17 18 19 20 | 21 inGTTTTCACTGGCGAGCGTCATCTTCCTACT 1. Identify the gene from which the query sequence originates (Name of the gene)2. Provide the FULL protein sequence encoded by the gene.3. Are different splice variants known for this gene?4. What human disease has been connected to this gene?5. Calculate molecular weight (kiloDalton, kD) and calculated pI (the pH where theprotein carries no net electrical charge) of the protein.6. Provide the reference (in proper reference form: Author; Year; Title; JournalName; Volume; Page Numbers) for a recent publication involving the identifiedgene. This reference should NOT be a web page reference.7. Are there homologs for the identified gene in other systems? Identify one homolog in an invertebrate system (if there is none, provide a vertebratehomolog).8. What is the function (e.g. transcriptional regulation, transmembrane signaling,kinase, protease, etc.) of the protein(s) encoded by the gene.9. Generate a FULL protein sequence alignment for one of the…
- GTTTTCACTGGCGAGCGTCATCTTCCTACT 8. What is the function (e.g. transcriptional regulation, transmembrane signaling, kinase, protease, etc.) of the protein(s) encoded by the gene.Question Which example is describing a "nonsense" mutation? O The normal amino acid sequence of a protein is Met-Ala-Phe-Tyr and the mutated allele produces an amino acid sequence Met-Ala-Phe-Leu O The normal amino acid sequence of a protein is Met-Ala-Phe Tyr and the mutated allele produces an amino acid sequence Met-Ala-Phe-Tyr O The normal amino acid sequence of a protein is Met-Ala-Phe-Tyr and the mutated allele produces an amino acid sequence Met-Ala-STOP Moire to the net question prevents changes to this angNLow-resolution X-ray diffraction analysis of a protein composed of long stretches of the sequence (-Gly-Ser-Gly-Ala-Gly-Ala-)n, where n indicates any number of repeats, shows an extended structure of stacked layers, with a repeat distance between layers that alternates between 3.5 Å and 5.7 Å. Propose a mođel that explains this scenario. 5. The right-hand panel in the linked figure shows sedimentation equilibrium analytical ultracentrifugation data for a mixture containing equimolar amounts of two fibrous proteins, Vps27 and Hsel. The blue circles are the data and the black line is the expected plot for a monodisperse 1:1 Vps27:Hsel complex of 23.7 kDa. In the left-hand panel, data is shown for Vps27 alone. The black line represents the expected curve for monomeric Vps27. Both experiments were run under identical conditions (same buffer, same spinning speed etc.) and the proteins have the same partial specific volume.