U heeft gezocht op: Adenosine

Catalogus nummer: (BOSSBS-13018R-CY7)

Leverancier: Bioss

Omschrijving: DNA polymerase activity is essential for replication, repair, recombination and mutagenesis. DNA polymerases can often bypass DNA lesions that block DNA replication, thereby allowing the replication of damaged DNA. One such DNA polymerase is the distributive enzyme DNA Pol i, which is encoded by the POLI gene. POLI is located on human chromosome 18q21.2, a region often implicated in the etiology of many human cancers. At thymine templates, DNA Pol i is highly error-prone when replicating undamaged DNA in that it favors the misincorporation of guanine over the correct nucleotide, adenosine. DNA Pol i also promotes the replication of damaged DNA by misincorporating deoxynucleotides opposite DNA lesions. DNA Pol i acts sequentially with DNA Pol Ω, which is essential for damage-induced mutagenesis, to complete the DNA lesion bypass. Therefore, replication involving DNA Pol i is likely to be highly mutagenic.

UOM: 1 * 100 µl

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Catalogus nummer: (BOSSBS-13018R-A647)

Leverancier: Bioss

Omschrijving: DNA polymerase activity is essential for replication, repair, recombination and mutagenesis. DNA polymerases can often bypass DNA lesions that block DNA replication, thereby allowing the replication of damaged DNA. One such DNA polymerase is the distributive enzyme DNA Pol i, which is encoded by the POLI gene. POLI is located on human chromosome 18q21.2, a region often implicated in the etiology of many human cancers. At thymine templates, DNA Pol i is highly error-prone when replicating undamaged DNA in that it favors the misincorporation of guanine over the correct nucleotide, adenosine. DNA Pol i also promotes the replication of damaged DNA by misincorporating deoxynucleotides opposite DNA lesions. DNA Pol i acts sequentially with DNA Pol Ω, which is essential for damage-induced mutagenesis, to complete the DNA lesion bypass. Therefore, replication involving DNA Pol i is likely to be highly mutagenic.

UOM: 1 * 100 µl

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Catalogus nummer: (BOSSBS-13018R-A680)

Leverancier: Bioss

Omschrijving: DNA polymerase activity is essential for replication, repair, recombination and mutagenesis. DNA polymerases can often bypass DNA lesions that block DNA replication, thereby allowing the replication of damaged DNA. One such DNA polymerase is the distributive enzyme DNA Pol i, which is encoded by the POLI gene. POLI is located on human chromosome 18q21.2, a region often implicated in the etiology of many human cancers. At thymine templates, DNA Pol i is highly error-prone when replicating undamaged DNA in that it favors the misincorporation of guanine over the correct nucleotide, adenosine. DNA Pol i also promotes the replication of damaged DNA by misincorporating deoxynucleotides opposite DNA lesions. DNA Pol i acts sequentially with DNA Pol , which is essential for damage-induced mutagenesis, to complete the DNA lesion bypass. Therefore, replication involving DNA Pol i is likely to be highly mutagenic.

UOM: 1 * 100 µl

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Catalogus nummer: (BOSSBS-13018R-A750)

Leverancier: Bioss

Omschrijving: DNA polymerase activity is essential for replication, repair, recombination and mutagenesis. DNA polymerases can often bypass DNA lesions that block DNA replication, thereby allowing the replication of damaged DNA. One such DNA polymerase is the distributive enzyme DNA Pol i, which is encoded by the POLI gene. POLI is located on human chromosome 18q21.2, a region often implicated in the etiology of many human cancers. At thymine templates, DNA Pol i is highly error-prone when replicating undamaged DNA in that it favors the misincorporation of guanine over the correct nucleotide, adenosine. DNA Pol i also promotes the replication of damaged DNA by misincorporating deoxynucleotides opposite DNA lesions. DNA Pol i acts sequentially with DNA Pol , which is essential for damage-induced mutagenesis, to complete the DNA lesion bypass. Therefore, replication involving DNA Pol i is likely to be highly mutagenic.

UOM: 1 * 100 µl

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Catalogus nummer: (PRSI4815)

Leverancier: ProSci Inc.

Omschrijving: HINT1 Antibody: Histidine triad nucleotide-binding protein 1 (HINT1) is a member of the histidine triad (HIT) protein family, a group of small nucleotide-binding and -hydrolyzing proteins. HINT1 interacts with several diverse proteins and has been suggested to have tumor suppressive activities. HINT1 catalyzes the hydrolysis of adenosine 5'-monophoramidate substrates such as AMP-morpholidate, but its enzymatic function does not appear to play a role in its tumor suppression. Recent experiments demonstrate that HINT1 forms a complex with POSH and JNK in vivo, inhibiting AP-1 activity and the phosphorylation of c-Jun, and this action could contribute to the tumor suppressor activity of HINT1. Other studies raise the possibility of HINT1 as a candidate gene for schizophrenia.

UOM: 1 * 1 EA

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Catalogus nummer: (BOSSBS-2167R-A555)

Leverancier: Bioss

Omschrijving: Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence.

UOM: 1 * 100 µl

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Catalogus nummer: (BOSSBS-2167R-CY3)

Leverancier: Bioss

Omschrijving: Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence.

UOM: 1 * 100 µl

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Catalogus nummer: (PRSI34-037)

Leverancier: ProSci Inc.

Omschrijving: Cystic fibrosis transmembrane conductance regulator (CFTR) is composed of two membrane-spanning domains (MSD), two nucleotide-binding domains (NBD), and an R domain. It is structurally similar to multidrug resistance (MDR1) protein and both are members of the superfamily of ATP-binding cassette (ABC) transporters, also known as traffic ATPases, which are implicated in the movement of various substrates. The protein is a small conductance adenosine 3',5'-cyclic monophosphate (cAMP)-activated chloride ion channel found in the apical membranes of epithelia within the pancreas, airway, intestine, bile duct, sweat gland, and male genital ducts. CFTR is a valuable marker of human pancreatic duct cell development and differentiation.

UOM: 1 * 1 EA

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Catalogus nummer: (PRSI92-367)

Leverancier: ProSci Inc.

Omschrijving: PAPSS1 is a bifunctional enzyme with both ATP sulfurylase and APS kinase activity. In the N-terminal section, it belongs to the APS kinase family; while the C-terminal section belongs to the sulfate adenylyltransferase family. PAPSS1 can be inhibited by chlorate, and is expressed in many tissues, such as high endothelial venules (HEV) cells and in cartilage. PAPSS1 mediates two steps in the sulfate activation pathway. The first step is the transfer of a sulfate group to ATP to yield adenosine 5'-phosphosulfate (APS), and the second step is the transfer of a phosphate group from ATP to APS yielding 3'-phosphoadenylylsulfate. In mammals, PAPS is the sole source of sulfate; APS appears to be only an intermediate in the sulfate-activation pathway. PAPSS1 also involved in the biosynthesis of sulfated L-selectin ligands in endothelial cells.

UOM: 1 * 1 EA

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Catalogus nummer: (PRSI33-773)

Leverancier: ProSci Inc.

Omschrijving: Cystic fibrosis transmembrane conductance regulator (CFTR) is composed of two membrane-spanning domains (MSD), two nucleotide-binding domains (NBD), and an R domain. It is structurally similar to multidrug resistance (MDR1) protein and both are members of the superfamily of ATP-binding cassette (ABC) transporters, also known as traffic ATPases, which are implicated in the movement of various substrates. The protein is a small conductance adenosine 3',5'-cyclic monophosphate (cAMP)-activated chloride ion channel found in the apical membranes of epithelia within the pancreas, airway, intestine, bile duct, sweat gland, and male genital ducts. CFTR is a valuable marker of human pancreatic duct cell development and differentiation.

UOM: 1 * 1 EA

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Catalogus nummer: (BOSSBS-2167R-A350)

Leverancier: Bioss

Omschrijving: Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence.

UOM: 1 * 100 µl

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Catalogus nummer: (BOSSBS-2167R-HRP)

Leverancier: Bioss

Omschrijving: Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence.

UOM: 1 * 100 µl

Sale

Catalogus nummer: (BOSSBS-2167R-CY7)

Leverancier: Bioss

Omschrijving: Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence.

UOM: 1 * 100 µl

Sale

Catalogus nummer: (BOSSBS-2167R-CY5.5)

Leverancier: Bioss

Omschrijving: Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence.

UOM: 1 * 100 µl

Sale

Catalogus nummer: (BOSSBS-2167R-FITC)

Leverancier: Bioss

Omschrijving: Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence.

UOM: 1 * 100 µl

Sale

Catalogus nummer: (BOSSBS-2167R-A750)

Leverancier: Bioss

Omschrijving: catalyses the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence.

UOM: 1 * 100 µl

Sale