PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 3609115-7 1987 In addition, TBC is influenced by the temperature-dependent hepatic metabolism of fentanyl. Fentanyl 82-90 TBC1 domain family member 1 Homo sapiens 13-16 34208471-0 2021 Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots? Fatty Acids 66-76 TBC1 domain family member 1 Homo sapiens 23-29 34208471-1 2021 TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Glucose 103-110 TBC1 domain family member 1 Homo sapiens 19-25 34208471-1 2021 TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. long chain fatty acids 141-163 TBC1 domain family member 1 Homo sapiens 19-25 34208471-1 2021 TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. lcfas 165-170 TBC1 domain family member 1 Homo sapiens 19-25 35192682-2 2022 This process depends on the redistribution of glucose transporters to the surface membrane, a process which involves regulatory proteins such as TBC1D1 and TBC1D4. Glucose 46-53 TBC1 domain family member 1 Homo sapiens 145-151 6619649-1 1983 This paper reports total body calcium by neutron activation (TBC) measurements in 94 normal individuals and 86 osteoporotic patients. Calcium 30-37 TBC1 domain family member 1 Homo sapiens 61-64 25280670-0 2015 Roles of TBC1D1 and TBC1D4 in insulin- and exercise-stimulated glucose transport of skeletal muscle. Glucose 63-70 TBC1 domain family member 1 Homo sapiens 9-15 33087848-2 2020 A key regulator of insulin- and exercise-stimulated glucose uptake and GLUT4 trafficking is TBC1D1. Glucose 52-59 TBC1 domain family member 1 Homo sapiens 92-98 33087848-4 2020 Using an unbiased quantitative proteomics approach, we identified proteins that interact with TBC1D1 in C2C12 myotubes including VPS13A and VPS13C, the Rab binding proteins EHBP1L1 and MICAL1, and the calcium pump SERCA1. Calcium 201-208 TBC1 domain family member 1 Homo sapiens 94-100 33087848-5 2020 These proteins associate with TBC1D1 via its phosphotyrosine binding (PTB) domains and their interactions with TBC1D1 were unaffected by AMPK activation, distinguishing them from the AMPK regulated interaction between TBC1D1 and AMPKalpha1 complexes. Phosphotyrosine 45-60 TBC1 domain family member 1 Homo sapiens 30-36 26822091-4 2016 Exercise increased AMPK alpha2beta2gamma3 activity and phosphorylation of ACCbeta Ser(221), TBC1D1 Ser(237)/Thr(596), and TBC1D4 Ser(704) Conversely, exercise decreased AMPK alpha1beta2gamma1 activity and TBC1D4 Ser(318)/Thr(642) phosphorylation. Serine 99-102 TBC1 domain family member 1 Homo sapiens 92-98 26822091-4 2016 Exercise increased AMPK alpha2beta2gamma3 activity and phosphorylation of ACCbeta Ser(221), TBC1D1 Ser(237)/Thr(596), and TBC1D4 Ser(704) Conversely, exercise decreased AMPK alpha1beta2gamma1 activity and TBC1D4 Ser(318)/Thr(642) phosphorylation. Serine 99-102 TBC1 domain family member 1 Homo sapiens 92-98 26822091-4 2016 Exercise increased AMPK alpha2beta2gamma3 activity and phosphorylation of ACCbeta Ser(221), TBC1D1 Ser(237)/Thr(596), and TBC1D4 Ser(704) Conversely, exercise decreased AMPK alpha1beta2gamma1 activity and TBC1D4 Ser(318)/Thr(642) phosphorylation. Serine 99-102 TBC1 domain family member 1 Homo sapiens 92-98 30945849-3 2019 In this study, we focused on geometric isomers cis- and trans-2,3-butylene carbonates ( c/ t-BC) as model electrolytes. Carbon 20-21 TBC1 domain family member 1 Homo sapiens 91-95 30945849-4 2019 Despite their similar structures and chemical properties, t-BC-based electrolytes have been reported to enable the reversible reaction of graphite anodes [as in ethylene carbonate (EC)], whereas c-BC-based electrolytes cause the exfoliation of graphite [as in propylene carbonate (PC)]. Graphite 138-146 TBC1 domain family member 1 Homo sapiens 58-62 30945849-4 2019 Despite their similar structures and chemical properties, t-BC-based electrolytes have been reported to enable the reversible reaction of graphite anodes [as in ethylene carbonate (EC)], whereas c-BC-based electrolytes cause the exfoliation of graphite [as in propylene carbonate (PC)]. ethylene carbonate 161-179 TBC1 domain family member 1 Homo sapiens 58-62 30945849-4 2019 Despite their similar structures and chemical properties, t-BC-based electrolytes have been reported to enable the reversible reaction of graphite anodes [as in ethylene carbonate (EC)], whereas c-BC-based electrolytes cause the exfoliation of graphite [as in propylene carbonate (PC)]. ethylene carbonate 181-183 TBC1 domain family member 1 Homo sapiens 58-62 30135087-2 2018 One target is TBC1D1 a Rab-GTPase-activating protein that regulates glucose uptake in muscle cells by integrating insulin signalling with that promoted by muscle contraction. Glucose 68-75 TBC1 domain family member 1 Homo sapiens 14-20 30135087-3 2018 Ser237 in TBC1D1 is a target for phosphorylation by AMPK, an event which may be important in regulating glucose uptake. Glucose 104-111 TBC1 domain family member 1 Homo sapiens 10-16 30135087-5 2018 The interaction between the two proteins is direct, involves a dual interaction mechanism employing both phosphotyrosine-binding (PTB) domains of TBC1D1 and is increased by two different pharmacological activators of AMPK (AICAR and A769962). Phosphotyrosine 105-120 TBC1 domain family member 1 Homo sapiens 146-152 29089333-7 2018 Key regulatory residues on the Rab-GAPs AS160 and TBC1D1 were phosphorylated in response to EPS. eps 92-95 TBC1 domain family member 1 Homo sapiens 50-56 25280670-1 2015 This review focuses on two paralogue Rab GTPase activating proteins known as TBC1D1 Tre-2/BUB2/cdc 1 domain family (TBC1D) 1 and TBC1D4 (also called Akt Substrate of 160 kDa, AS160) and their roles in controlling skeletal muscle glucose transport in response to the independent and combined effects of insulin and exercise. Glucose 229-236 TBC1 domain family member 1 Homo sapiens 77-83 25280670-1 2015 This review focuses on two paralogue Rab GTPase activating proteins known as TBC1D1 Tre-2/BUB2/cdc 1 domain family (TBC1D) 1 and TBC1D4 (also called Akt Substrate of 160 kDa, AS160) and their roles in controlling skeletal muscle glucose transport in response to the independent and combined effects of insulin and exercise. Glucose 229-236 TBC1 domain family member 1 Homo sapiens 116-124 25280670-3 2015 TBC1D1 phosphorylation on several insulin-responsive sites (including T596, a site corresponding to T642 in TBC1D4) does not appear to be essential for in vivo insulin-stimulated glucose uptake by skeletal muscle. t596 70-74 TBC1 domain family member 1 Homo sapiens 0-6 25280670-4 2015 In vivo exercise or ex vivo contraction of muscle result in greater TBC1D1 phosphorylation on S237 that is likely to be secondary to increased AMP-activated protein kinase activity and potentially important for contraction-stimulated glucose uptake. Glucose 234-241 TBC1 domain family member 1 Homo sapiens 68-74 25280670-8 2015 In summary, TBC1D1 and TBC1D4 have important, but distinct roles in regulating muscle glucose transport in response to insulin and exercise. Glucose 86-93 TBC1 domain family member 1 Homo sapiens 12-18 24879834-0 2014 The adaptor protein APPL2 inhibits insulin-stimulated glucose uptake by interacting with TBC1D1 in skeletal muscle. Glucose 54-61 TBC1 domain family member 1 Homo sapiens 89-95 24879834-7 2014 Insulin stimulates TBC1D1 phosphorylation on serine 235, leading to enhanced interaction with the BAR domain of APPL2, which in turn suppresses insulin-evoked TBC1D1 phosphorylation on threonine 596 in cultured myotubes and skeletal muscle. Serine 45-51 TBC1 domain family member 1 Homo sapiens 19-25 24879834-8 2014 Substitution of serine 235 with alanine diminishes APPL2-mediated inhibition on insulin-dependent TBC1D1 phosphorylation on threonine 596 and the suppressive effects of TBC1D1 on insulin-induced glucose uptake and GLUT4 translocation to the plasma membrane in cultured myotubes. Threonine 124-133 TBC1 domain family member 1 Homo sapiens 98-104 24879834-8 2014 Substitution of serine 235 with alanine diminishes APPL2-mediated inhibition on insulin-dependent TBC1D1 phosphorylation on threonine 596 and the suppressive effects of TBC1D1 on insulin-induced glucose uptake and GLUT4 translocation to the plasma membrane in cultured myotubes. Glucose 195-202 TBC1 domain family member 1 Homo sapiens 169-175 24879834-9 2014 Therefore, the APPL2-TBC1D1 interaction is a key step to fine tune insulin-stimulated glucose uptake by regulating the membrane recruitment of GLUT4 in skeletal muscle. Glucose 86-93 TBC1 domain family member 1 Homo sapiens 21-27 24879834-7 2014 Insulin stimulates TBC1D1 phosphorylation on serine 235, leading to enhanced interaction with the BAR domain of APPL2, which in turn suppresses insulin-evoked TBC1D1 phosphorylation on threonine 596 in cultured myotubes and skeletal muscle. Serine 45-51 TBC1 domain family member 1 Homo sapiens 159-165 24879834-7 2014 Insulin stimulates TBC1D1 phosphorylation on serine 235, leading to enhanced interaction with the BAR domain of APPL2, which in turn suppresses insulin-evoked TBC1D1 phosphorylation on threonine 596 in cultured myotubes and skeletal muscle. Threonine 185-194 TBC1 domain family member 1 Homo sapiens 19-25 24879834-7 2014 Insulin stimulates TBC1D1 phosphorylation on serine 235, leading to enhanced interaction with the BAR domain of APPL2, which in turn suppresses insulin-evoked TBC1D1 phosphorylation on threonine 596 in cultured myotubes and skeletal muscle. Threonine 185-194 TBC1 domain family member 1 Homo sapiens 159-165 24492152-7 2014 The experimental results show that COD, DO and the concentration of fecal coliform vary a little with the changing of water temperature; TBC increases dramatically when the water temperature is over 16 C; and TBC in summer is 30 times more than that in winter. Water 118-123 TBC1 domain family member 1 Homo sapiens 137-140 24492152-7 2014 The experimental results show that COD, DO and the concentration of fecal coliform vary a little with the changing of water temperature; TBC increases dramatically when the water temperature is over 16 C; and TBC in summer is 30 times more than that in winter. Water 118-123 TBC1 domain family member 1 Homo sapiens 210-213 24492152-7 2014 The experimental results show that COD, DO and the concentration of fecal coliform vary a little with the changing of water temperature; TBC increases dramatically when the water temperature is over 16 C; and TBC in summer is 30 times more than that in winter. Water 173-178 TBC1 domain family member 1 Homo sapiens 137-140 24492152-7 2014 The experimental results show that COD, DO and the concentration of fecal coliform vary a little with the changing of water temperature; TBC increases dramatically when the water temperature is over 16 C; and TBC in summer is 30 times more than that in winter. Water 173-178 TBC1 domain family member 1 Homo sapiens 210-213 25495476-4 2014 Employing C. elegans and human primary fibroblasts, we show that RAB3GAP1 and RAB3GAP2, which are components of the TBC domain-free RAB3GAP complex, influence protein aggregation and affect autophagy at basal and rapamycin-induced conditions. Sirolimus 213-222 TBC1 domain family member 1 Homo sapiens 116-119 24247980-1 2014 We investigated the phosphorylation signatures of two Rab-GTPase activating proteins TBC1D1 and TBC1D4 in human skeletal muscle in response to physical exercise and physiological insulin levels induced by a carbohydrate rich meal using a paired experimental design. Carbohydrates 207-219 TBC1 domain family member 1 Homo sapiens 85-91 23752133-2 2013 Animal and cell culture experiments have shown that site-specific phosphorylation of the Rab-GTPase-activating proteins AS160 and TBC1D1 is critical for GLUT4 translocation facilitating glucose uptake, but their regulation in human skeletal muscle is not well understood. Glucose 186-193 TBC1 domain family member 1 Homo sapiens 130-136 23752133-6 2013 Interestingly, insulin-stimulated phosphorylation of TBC1D1 Thr(590), a site shown to be regulated by insulin in rodents, was only increased in T2D subjects, although the functional significance of this difference is unknown. Threonine 60-63 TBC1 domain family member 1 Homo sapiens 53-59 23667688-3 2013 A non-synonymous polymorphism (rs35859249, p.Arg125Trp) in the N-terminal TBC1D1 phosphotyrosine-binding (PTB) domain has shown a replicated association with familial obesity in women. Phosphotyrosine 81-96 TBC1 domain family member 1 Homo sapiens 74-80 23364847-4 2013 METHODS: We analyzed rs9852 and rs35859249 in TBC1D1 in 195 schizophrenia subjects treated mostly with clozapine or olanzapine for up to 14 weeks. Clozapine 103-112 TBC1 domain family member 1 Homo sapiens 46-52 23364847-4 2013 METHODS: We analyzed rs9852 and rs35859249 in TBC1D1 in 195 schizophrenia subjects treated mostly with clozapine or olanzapine for up to 14 weeks. Olanzapine 116-126 TBC1 domain family member 1 Homo sapiens 46-52 23325788-2 2013 By using GLUT4 nanometry combined with a cell-based reconstitution model, we uncover a shift in the regulatory mode of Tbc1d1 by showing that Tbc1d1 temporally acquires insulin responsiveness, which triggers GLUT4 trafficking only after an exercise-mimetic stimulus such as aminoimidazole carboxamide ribonucleotide (AICAR) pretreatment. AICA ribonucleotide 274-315 TBC1 domain family member 1 Homo sapiens 119-125 23325788-2 2013 By using GLUT4 nanometry combined with a cell-based reconstitution model, we uncover a shift in the regulatory mode of Tbc1d1 by showing that Tbc1d1 temporally acquires insulin responsiveness, which triggers GLUT4 trafficking only after an exercise-mimetic stimulus such as aminoimidazole carboxamide ribonucleotide (AICAR) pretreatment. AICA ribonucleotide 274-315 TBC1 domain family member 1 Homo sapiens 142-148 22241155-5 2011 We show a case of a 39-year-old woman with recurrent CNS involvement of IVLBCL receiving autologous peripheral blood stem cell transplantation (auto-PBSCT) preconditioned with high-dose thiotepa, busulfan, cyclophosphamide (TBC regimen). Thiotepa 186-194 TBC1 domain family member 1 Homo sapiens 224-227 23325788-2 2013 By using GLUT4 nanometry combined with a cell-based reconstitution model, we uncover a shift in the regulatory mode of Tbc1d1 by showing that Tbc1d1 temporally acquires insulin responsiveness, which triggers GLUT4 trafficking only after an exercise-mimetic stimulus such as aminoimidazole carboxamide ribonucleotide (AICAR) pretreatment. AICA ribonucleotide 317-322 TBC1 domain family member 1 Homo sapiens 119-125 23325788-2 2013 By using GLUT4 nanometry combined with a cell-based reconstitution model, we uncover a shift in the regulatory mode of Tbc1d1 by showing that Tbc1d1 temporally acquires insulin responsiveness, which triggers GLUT4 trafficking only after an exercise-mimetic stimulus such as aminoimidazole carboxamide ribonucleotide (AICAR) pretreatment. AICA ribonucleotide 317-322 TBC1 domain family member 1 Homo sapiens 142-148 22396207-8 2012 Furthermore, CR-induced activation of Akt-TBC1D1/TBC1D4 signaling, inhibition of mammalian target of rapamycin-S6K1-insulin receptor substrate-1 pathway, and induction of nicotinamide phosphoribosyltransferase-NAD(+)-sirtuin-1 cascade were remarkably impaired in AMPK-alpha2(-/-) mice. Chromium 13-15 TBC1 domain family member 1 Homo sapiens 42-48 22391950-3 2012 Acute aerobic exercise first accelerates translocation of myocellular glucose transporters via AMP-activated protein kinase, calcium release and mitogen-activated protein kinase, but also improves insulin-dependent glucose transport/phosphorylation via distal components of insulin signalling (phosphoinositide-dependent kinase 1, TBC1 domain family, members 1 and 4, Rac1, protein kinase C). Glucose 70-77 TBC1 domain family member 1 Homo sapiens 331-335 22241155-5 2011 We show a case of a 39-year-old woman with recurrent CNS involvement of IVLBCL receiving autologous peripheral blood stem cell transplantation (auto-PBSCT) preconditioned with high-dose thiotepa, busulfan, cyclophosphamide (TBC regimen). Cyclophosphamide 206-222 TBC1 domain family member 1 Homo sapiens 224-227 19740738-5 2009 We show that a mutant of TBC1D1, in which several Akt sites have been converted to alanine, is considerably more inhibitory to insulin-stimulated GLUT4 translocation than wild-type TBC1D1. Alanine 83-90 TBC1 domain family member 1 Homo sapiens 25-31 21871813-4 2011 They interact with the Rab GTPase-activating proteins AS160 and TBC1D1 to regulate glucose uptake into target tissues in response to insulin and energy stress. Glucose 83-90 TBC1 domain family member 1 Homo sapiens 64-70 21505148-2 2011 Studies in rodents demonstrate that the underlying mechanism for glucose uptake in muscle involves site-specific phosphorylation of the Rab-GTPase-activating proteins AS160 (TBC1D4) and TBC1D1. Glucose 65-72 TBC1 domain family member 1 Homo sapiens 186-192 21505148-8 2011 Muscle lysates were analyzed for AMPK activity and Akt phosphorylation and for TBC1D1 and AS160 phosphorylation on known or putative AMPK and Akt sites as follows: AS160 Ser(711) (AMPK), TBC1D1 Ser(231) (AMPK), TBC1D1 Ser(660) (AMPK), TBC1D1 Ser(700) (AMPK), and TBC1D1 Thr(590) (Akt). Serine 170-173 TBC1 domain family member 1 Homo sapiens 79-85 21454505-4 2011 We further tested the relevance of this model by Ala-scanning mutagenesis, but only one of five substitutions within the inferred binding site of the TBC1D1 RabGAP significantly perturbed catalytic efficiency. Alanine 49-52 TBC1 domain family member 1 Homo sapiens 150-156 21454505-7 2011 Ala substitution of TBC1D1 Met(930), corresponding to a residue outside of the Gyp1p/Rab33B contact, substantially reduced catalytic activity. Alanine 0-3 TBC1 domain family member 1 Homo sapiens 20-26 19955868-1 2009 Akt substrate of 160 kDa (called AS160 or TBC1D4) and TBC1D1, Rab GTPase-activating proteins that regulate glucose transport, become phosphorylated with exercise or insulin stimulation. Glucose 107-114 TBC1 domain family member 1 Homo sapiens 54-60 10965142-1 2000 TBC1D1 is the founding member of a family of related proteins with homology to tre-2/UPS6, BUB2, and cdc16 and containing the tbc box motif of 180-220 amino acids. Tubercidin 126-129 TBC1 domain family member 1 Homo sapiens 0-6 18780777-3 2008 Tbc1d1, a Rab-GAP implicated in exercise-induced GLUT4 translocation in skeletal muscle, also appeared to be phosphorylated on Ser(231) after EPS-induced contraction. Serine 127-130 TBC1 domain family member 1 Homo sapiens 0-6 16923123-5 2006 Systematic investigation of 2400 combinations of 60 GTP-fixed Rabs and 40 TBC proteins by yeast two-hybrid screening revealed that seven TBC proteins specifically and differentially interact with specific Rabs (e.g. OATL1 interacts with Rab2A; FLJ12085 with Rab5A/B/C; and Evi5-like with Rab10). Guanosine Triphosphate 52-55 TBC1 domain family member 1 Homo sapiens 137-140 18215134-7 2008 Remarkably, loss of TBC1D1 in 3T3-L1 adipocytes activated the mTOR (mammalian target of rapamycin)-p70 S6 protein kinase pathway, and the increase in GLUT1 expression in the cells treated with TBC1D1 siRNA (small interfering RNA) was blocked by the mTOR inhibitor rapamycin. Sirolimus 88-97 TBC1 domain family member 1 Homo sapiens 20-26 18215134-8 2008 Furthermore, overexpression of the mutant TBC1D1-T590A, lacking the putative Akt/PKB phosphorylation site, inhibited insulin stimulation of p70 S6 kinase phosphorylation at Thr(389), a phosphorylation induced by mTOR. Threonine 173-176 TBC1 domain family member 1 Homo sapiens 42-48 18258599-8 2008 In addition, we discovered that Tbc1d1 is much more highly expressed in skeletal muscle than fat and that the AMP-activated protein kinase (AMPK) activator 5"-aminoimidazole-4-carboxamide ribonucleoside partially reversed the inhibition of insulin-stimulated GLUT4 translocation by overexpressed Tbc1d1 in 3T3-L1 adipocytes. acadesine 156-202 TBC1 domain family member 1 Homo sapiens 32-38 18258599-8 2008 In addition, we discovered that Tbc1d1 is much more highly expressed in skeletal muscle than fat and that the AMP-activated protein kinase (AMPK) activator 5"-aminoimidazole-4-carboxamide ribonucleoside partially reversed the inhibition of insulin-stimulated GLUT4 translocation by overexpressed Tbc1d1 in 3T3-L1 adipocytes. acadesine 156-202 TBC1 domain family member 1 Homo sapiens 296-302 17995453-3 2008 TBC1D1 has two clusters of phosphorylated residues, either side of the second PTB (phosphotyrosine-binding domain). Phosphotyrosine 83-98 TBC1 domain family member 1 Homo sapiens 0-6 17995453-6 2008 In HEK-293 cells, LY294002 inhibits phosphorylation of Thr596 of TBC1D1, and promotes phosphorylation of AMPK and Ser237 of TBC1D1. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 18-26 TBC1 domain family member 1 Homo sapiens 65-71 17995453-6 2008 In HEK-293 cells, LY294002 inhibits phosphorylation of Thr596 of TBC1D1, and promotes phosphorylation of AMPK and Ser237 of TBC1D1. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 18-26 TBC1 domain family member 1 Homo sapiens 124-130 12009413-1 2002 The stoichiometry of oxygen consumption during tyrosinase-catalyzed oxidation of an o-diphenol (4-tert-butylcatechol, TBC) and a monophenol (4-tert-butylphenol, TBP) has been determined. Oxygen 21-27 TBC1 domain family member 1 Homo sapiens 118-121 12009413-1 2002 The stoichiometry of oxygen consumption during tyrosinase-catalyzed oxidation of an o-diphenol (4-tert-butylcatechol, TBC) and a monophenol (4-tert-butylphenol, TBP) has been determined. catechol 84-94 TBC1 domain family member 1 Homo sapiens 118-121 9692212-2 1998 The sequences of the TBC-1 and TBC-2 were solved by analysis of peptides derived by enzymatic digestions as well as by chemical cleavages with cyanogen bromide (CNBr), o-iodosobenzoic acid, and hydroxylamine. Cyanogen Bromide 143-159 TBC1 domain family member 1 Homo sapiens 21-26 9692212-2 1998 The sequences of the TBC-1 and TBC-2 were solved by analysis of peptides derived by enzymatic digestions as well as by chemical cleavages with cyanogen bromide (CNBr), o-iodosobenzoic acid, and hydroxylamine. Cyanogen Bromide 161-165 TBC1 domain family member 1 Homo sapiens 21-26 9692212-2 1998 The sequences of the TBC-1 and TBC-2 were solved by analysis of peptides derived by enzymatic digestions as well as by chemical cleavages with cyanogen bromide (CNBr), o-iodosobenzoic acid, and hydroxylamine. Hydroxylamine 194-207 TBC1 domain family member 1 Homo sapiens 21-26