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Ace+Method+Development+Kits
Numéro de catalogue:
(BOSSBS-11693R-HRP)
Fournisseur:
Bioss
Description:
Probable RNA/DNA helicase involved in diverse aspects of RNA metabolism and genomic integrity. Plays a role in transcription regulation by its ability to modulate RNA Polymerase II (Pol II) binding to chromatin and through its interaction with proteins involved in transcription (PubMed:19515850, PubMed:21700224). Contributes to the mRNA splicing efficiency and splice site selection (PubMed:19515850). Required for the resolution of R-loop RNA-DNA hybrid formation at G-rich pause sites located downstream of the poly(A) site, allowing XRN2 recruitment and XRN2-mediated degradation of the downstream cleaved RNA and hence efficient RNA polymerase II (RNAp II) transcription termination (PubMed:19515850, PubMed:21700224). Required for the 3' transcriptional termination of PER1 and CRY2, thus playing an important role in the circadian rhythm regulation (By similarity). Involved in DNA double-strand breaks damage response generated by oxidative stress (PubMed:17562789). In association with RRP45, targets the RNA exosome complex to sites of transcription-induced DNA damage (PubMed:24105744). Plays a role in the development and maturation of germ cells: essential for male meiosis, acting at the interface of transcription and meiotic recombination, and in the process of gene silencing during meiotic sex chromosome inactivation (MSCI) (By similarity). May be involved in telomeric stability through the regulation of telomere repeat-containing RNA (TERRA) transcription (PubMed:21112256). Plays a role in neurite outgrowth in hippocampal cells through FGF8-activated signaling pathways. Inhibits retinoic acid-induced apoptosis (PubMed:21576111).
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-11693R-CY3)
Fournisseur:
Bioss
Description:
Probable RNA/DNA helicase involved in diverse aspects of RNA metabolism and genomic integrity. Plays a role in transcription regulation by its ability to modulate RNA Polymerase II (Pol II) binding to chromatin and through its interaction with proteins involved in transcription (PubMed:19515850, PubMed:21700224). Contributes to the mRNA splicing efficiency and splice site selection (PubMed:19515850). Required for the resolution of R-loop RNA-DNA hybrid formation at G-rich pause sites located downstream of the poly(A) site, allowing XRN2 recruitment and XRN2-mediated degradation of the downstream cleaved RNA and hence efficient RNA polymerase II (RNAp II) transcription termination (PubMed:19515850, PubMed:21700224). Required for the 3' transcriptional termination of PER1 and CRY2, thus playing an important role in the circadian rhythm regulation (By similarity). Involved in DNA double-strand breaks damage response generated by oxidative stress (PubMed:17562789). In association with RRP45, targets the RNA exosome complex to sites of transcription-induced DNA damage (PubMed:24105744). Plays a role in the development and maturation of germ cells: essential for male meiosis, acting at the interface of transcription and meiotic recombination, and in the process of gene silencing during meiotic sex chromosome inactivation (MSCI) (By similarity). May be involved in telomeric stability through the regulation of telomere repeat-containing RNA (TERRA) transcription (PubMed:21112256). Plays a role in neurite outgrowth in hippocampal cells through FGF8-activated signaling pathways. Inhibits retinoic acid-induced apoptosis (PubMed:21576111).
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-6929R)
Fournisseur:
Bioss
Description:
Required for the cytoplasmic dynein-driven retrograde movement of vesicles and organelles along microtubules. Dynein-dynactin interaction is a key component of the mechanism of axonal transport of vesicles and organelles.Tissue specificity; Brain.Involvement in disease; Defects in DCTN1 are the cause of distal hereditary motor neuronopathy type 7B (HMN7B); also known as progressive lower motor neuron disease (PLMND). HMN7B is a neuromuscular disorder. Distal hereditary motor neuronopathies constitute a heterogeneous group of neuromuscular disorders caused by selective degeneration of motor neurons in the anterior horn of the spinal cord, without sensory deficit in the posterior horn. The overall clinical picture consists of a classical distal muscular atrophy syndrome in the legs without clinical sensory loss. The disease starts with weakness and wasting of distal muscles of the anterior tibial and peroneal compartments of the legs. Later on, weakness and atrophy may expand to the proximal muscles of the lower limbs and/or to the distal upper limbs.Defects in DCTN1 are a cause of susceptibility to amyotrophic lateral sclerosis (ALS). ALS is a neurodegenerative disorder affecting upper and lower motor neurons, and resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology is likely to be multifactorial, involving both genetic and environmental factors.Defects in DCTN1 are the cause of Perry syndrome (PERRYS); also called parkinsonism with alveolar hypoventilation and mental depression. Perry syndrome is a neuropsychiatric disorder characterized by mental depression not responsive to antidepressant drugs or electroconvulsive therapy, sleep disturbances, exhaustion and marked weight loss. Parkinsonism develops later and respiratory failure occurred terminally.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-1370R-A488)
Fournisseur:
Bioss
Description:
Serine/threonine protein kinase which activates checkpoint signaling upon double strand breaks (DSBs), apoptosis and genotoxic stresses such as ionizing ultraviolet A light (UVA), thereby acting as a DNA damage sensor. recognises the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at double strand breaks (DSBs), thereby regulating DNA damage response mechanism. Also plays a role in pre-B cell allelic exclusion, a process leading to expression of a single immunoglobulin heavy chain allele to enforce clonality and monospecific recognition by the B-cell antigen receptor (BCR) expressed on individual B-lymphocytes. After the introduction of DNA breaks by the RAG complex on one immunoglobulin allele, acts by mediating a repositioning of the second allele to pericentromeric heterochromatin, preventing accessibility to the RAG complex and recombination of the second allele. Also involved in signal transduction and cell cycle control. May function as a tumor suppressor. Necessary for activation of ABL1 and SAPK. Phosphorylates DYRK2, CHEK2, p53/TP53, FANCD2, NFKBIA, BRCA1, CTIP, nibrin (NBN), TERF1, RAD9 and DCLRE1C. May play a role in vesicle and/or protein transport. Could play a role in T-cell development, gonad and neurological function. Binds DNA ends. Plays a role in replication-dependent histone mRNA degradation. Phosphorylation of DYRK2 in nucleus in response to genotoxic stress prevents its MDM2-mediated ubiquitination and subsequent proteasome degradation. Phosphorylates ATF2 which stimulates its function in DNA damage response.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-6929R-A750)
Fournisseur:
Bioss
Description:
Required for the cytoplasmic dynein-driven retrograde movement of vesicles and organelles along microtubules. Dynein-dynactin interaction is a key component of the mechanism of axonal transport of vesicles and organelles.Tissue specificity; Brain.Involvement in disease; Defects in DCTN1 are the cause of distal hereditary motor neuronopathy type 7B (HMN7B); also known as progressive lower motor neuron disease (PLMND). HMN7B is a neuromuscular disorder. Distal hereditary motor neuronopathies constitute a heterogeneous group of neuromuscular disorders caused by selective degeneration of motor neurons in the anterior horn of the spinal cord, without sensory deficit in the posterior horn. The overall clinical picture consists of a classical distal muscular atrophy syndrome in the legs without clinical sensory loss. The disease starts with weakness and wasting of distal muscles of the anterior tibial and peroneal compartments of the legs. Later on, weakness and atrophy may expand to the proximal muscles of the lower limbs and/or to the distal upper limbs.Defects in DCTN1 are a cause of susceptibility to amyotrophic lateral sclerosis (ALS). ALS is a neurodegenerative disorder affecting upper and lower motor neurons, and resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology is likely to be multifactorial, involving both genetic and environmental factors.Defects in DCTN1 are the cause of Perry syndrome (PERRYS); also called parkinsonism with alveolar hypoventilation and mental depression. Perry syndrome is a neuropsychiatric disorder characterised by mental depression not responsive to antidepressant drugs or electroconvulsive therapy, sleep disturbances, exhaustion and marked weight loss. Parkinsonism develops later and respiratory failure occurred terminally.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3821R-A680)
Fournisseur:
Bioss
Description:
Histone demethylase that demethylates both 'Lys-4' (H3K4me) and 'Lys-9' (H3K9me) of histone H3, thereby acting as a coactivator or a corepressor, depending on the context. Acts by oxidising the substrate by FAD to generate the corresponding imine that is subsequently hydrolysed. Acts as a corepressor by mediating demethylation of H3K4me, a specific tag for epigenetic transcriptional activation. Demethylates both mono- (H3K4me1) and di-methylated (H3K4me2) H3K4me. May play a role in the repression of neuronal genes. Alone, it is unable to demethylate H3K4me on nucleosomes and requires the presence of RCOR1/CoREST to achieve such activity. Also acts as a coactivator of androgen receptor (ANDR)-dependent transcription, by being recruited to ANDR target genes and mediating demethylation of H3K9me, a specific tag for epigenetic transcriptional repression. The presence of PRKCB in ANDR-containing complexes, which mediates phosphorylation of 'Thr-6' of histone H3 (H3T6ph), a specific tag that prevents demethylation H3K4me, prevents H3K4me demethylase activity of KDM1A. Demethylates di-methylated 'Lys-370' of p53/TP53 which prevents interaction of p53/TP53 with TP53BP1 and represses p53/TP53-mediated transcriptional activation. Demethylates and stabilises the DNA methylase DNMT1. Required for gastrulation during embryogenesis. Component of a RCOR/GFI/KDM1A/HDAC complex that suppresses, via histone deacetylase (HDAC) recruitment, a number of genes implicated in multilineage blood cell development. Effector of SNAI1-mediated transcription repression of E-cadherin/CDH1, CDN7 and KRT8. Required for the maintenance of the silenced state of the SNAI1 target genes E-cadherin/CDH1 and CDN7.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3821R-CY7)
Fournisseur:
Bioss
Description:
Histone demethylase that demethylates both 'Lys-4' (H3K4me) and 'Lys-9' (H3K9me) of histone H3, thereby acting as a coactivator or a corepressor, depending on the context. Acts by oxidizing the substrate by FAD to generate the corresponding imine that is subsequently hydrolyzed. Acts as a corepressor by mediating demethylation of H3K4me, a specific tag for epigenetic transcriptional activation. Demethylates both mono- (H3K4me1) and di-methylated (H3K4me2) H3K4me. May play a role in the repression of neuronal genes. Alone, it is unable to demethylate H3K4me on nucleosomes and requires the presence of RCOR1/CoREST to achieve such activity. Also acts as a coactivator of androgen receptor (ANDR)-dependent transcription, by being recruited to ANDR target genes and mediating demethylation of H3K9me, a specific tag for epigenetic transcriptional repression. The presence of PRKCB in ANDR-containing complexes, which mediates phosphorylation of 'Thr-6' of histone H3 (H3T6ph), a specific tag that prevents demethylation H3K4me, prevents H3K4me demethylase activity of KDM1A. Demethylates di-methylated 'Lys-370' of p53/TP53 which prevents interaction of p53/TP53 with TP53BP1 and represses p53/TP53-mediated transcriptional activation. Demethylates and stabilizes the DNA methylase DNMT1. Required for gastrulation during embryogenesis. Component of a RCOR/GFI/KDM1A/HDAC complex that suppresses, via histone deacetylase (HDAC) recruitment, a number of genes implicated in multilineage blood cell development. Effector of SNAI1-mediated transcription repression of E-cadherin/CDH1, CDN7 and KRT8. Required for the maintenance of the silenced state of the SNAI1 target genes E-cadherin/CDH1 and CDN7.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3821R-CY3)
Fournisseur:
Bioss
Description:
Histone demethylase that demethylates both 'Lys-4' (H3K4me) and 'Lys-9' (H3K9me) of histone H3, thereby acting as a coactivator or a corepressor, depending on the context. Acts by oxidizing the substrate by FAD to generate the corresponding imine that is subsequently hydrolyzed. Acts as a corepressor by mediating demethylation of H3K4me, a specific tag for epigenetic transcriptional activation. Demethylates both mono- (H3K4me1) and di-methylated (H3K4me2) H3K4me. May play a role in the repression of neuronal genes. Alone, it is unable to demethylate H3K4me on nucleosomes and requires the presence of RCOR1/CoREST to achieve such activity. Also acts as a coactivator of androgen receptor (ANDR)-dependent transcription, by being recruited to ANDR target genes and mediating demethylation of H3K9me, a specific tag for epigenetic transcriptional repression. The presence of PRKCB in ANDR-containing complexes, which mediates phosphorylation of 'Thr-6' of histone H3 (H3T6ph), a specific tag that prevents demethylation H3K4me, prevents H3K4me demethylase activity of KDM1A. Demethylates di-methylated 'Lys-370' of p53/TP53 which prevents interaction of p53/TP53 with TP53BP1 and represses p53/TP53-mediated transcriptional activation. Demethylates and stabilizes the DNA methylase DNMT1. Required for gastrulation during embryogenesis. Component of a RCOR/GFI/KDM1A/HDAC complex that suppresses, via histone deacetylase (HDAC) recruitment, a number of genes implicated in multilineage blood cell development. Effector of SNAI1-mediated transcription repression of E-cadherin/CDH1, CDN7 and KRT8. Required for the maintenance of the silenced state of the SNAI1 target genes E-cadherin/CDH1 and CDN7.
UOM:
1 * 100 µl
Numéro de catalogue:
(ENZOADI905813100)
Fournisseur:
ENZO LIFE SCIENCES
Description:
The octapeptide circulatory hormone Angiotensin II is a critical regulator of cardiovascular homeostasis formed in blood, with dual function in tissues of the brain, kidney, heart, and vasculature as an autocrine/paracrine growth hormone. The actions of angiotensin II are mediated by type one (AT1) and type two (AT2) angiotensin II receptors, members of the seven-transmembrane Gprotein coupled receptor (GPCR) family. AT1 receptors couple predominantly with Gq/11 alpha subunits, and signal through phospholipases C, D, and A2, inositol phosphates, and calcium channels, as well as a variety of serine/threonine and tyrosine kinases. AT1 expression is greatest in vascular smooth muscle, liver, kidney, adrenal cortex, brain, and lung, and is primarily responsible for the physiological effects of angiotensin II, including regulation of arterial blood pressure, electrolyte and water balance, thirst, hormone secretion, and renal function. The AT2 receptor displays approximately 30% identity to the AT1 receptor, and is highly expressed during embryonic development. AT2 expression in adult tissue is limited to the adrenal medulla, brain, and reproductive tissues, but is upregulated in injured tissue following myocardial infarction, vascular injury, and wound healing. AT2 receptor signaling is not dependent on G-protein coupling or receptor phosphorylation, although coupling to Gia2 and Gia3 alpha subunits occurs in some tissues. AT2 activation can stimulate tyrosine and serine/threonine phosphatases through activation of nitric oxide and cGMP, and appears to counteract the stimulatory effects of AT1 receptor and growth factor receptor signaling.
UOM:
1 * 1 EA
New Product
Numéro de catalogue:
(720-1867)
Fournisseur:
Simport Scientific
Description:
L'entonnoir MEGA CytoSep™ permet de produire des préparations de lames minces de grande qualité de façon simple, efficace et économique.
Avec lui, plus besoin de clips en acier inoxydable, ce qui permet d'améliorer le flux de travail du laboratoire. Il est fait pour la préparation pratique de plus grands volumes d'échantillons. Ce grand entonnoir est facile et rapide à retirer. La grande zone de dépôt de cellules rectangulaire de 22×14,75 mm (325 mm² carré) accueille jusqu'à 12 fois le volume d'échantillons (6 ml) de l'entonnoir cytologique simple CytoSep™. Il permet de produire des préparations minces plus économiques par rapport à d'autres méthodes à couche mince. Le positionnement stratégique des baffles évite l'agglomération des cellules, ce qui permet une disposition uniforme de ces dernières et des préparations de lames d'excellente qualité. L'entonnoir cytologique MEGA CytoSep™ et le bouchon minimisent l'exposition de l'utilisateur aux agents pathogènes tout en réduisant le risque de contamination croisée des échantillons. Ils permettent de préparer des préparations séchées à l'air ou fixées.
UOM:
1 * 480 ST
Numéro de catalogue:
(BOSSBS-12495R-A750)
Fournisseur:
Bioss
Description:
APOBEC proteins inhibit retroviruses by deaminating cytosine residues of viral RNA and DNA. The seven APOBEC3 genes or pseudogenes are found in a cluster thought to result from gene duplication on chromosome 22. Like APOBEC3G, APOBEC3F deaminates deoxycytosine to deoxyuracil in the minus strand of HIV-1 DNA, resulting in G to A hypermutation in the plus strand of DNA. Thus, APOBEC3G and APOBEC3F provide a mechanism for innate immunity to retroviruses, and are also likely contribute to sequence variation observed in many viruses. Viral infectivity factor (Vif) imparts APOBEC3G and APOBEC3F resistance to HIV through impaired translation of their mRNA and accelerated posttranslational degradation of the APOBEC3 proteins by the 26S proteasome. Interestingly, HIV-1 Vif cannot form a complex with APOBEC3G or APOBEC3F of mouse origin as it does with the human protein, and thus mouse APOBEC3G and APOBEC3F function as a potent inhibitors of wildtype HIV-1 replication, where human APOBEC3G and APOBEC3F are only able to inhibit Vif-deficient HIV-1 replication. This implies that induction of APOBEC3G and APOBEC3F activity or a method of blocking their interaction with Vif may provide a method for therapeutic intervention.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12495R-A680)
Fournisseur:
Bioss
Description:
APOBEC proteins inhibit retroviruses by deaminating cytosine residues of viral RNA and DNA. The seven APOBEC3 genes or pseudogenes are found in a cluster thought to result from gene duplication on chromosome 22. Like APOBEC3G, APOBEC3F deaminates deoxycytosine to deoxyuracil in the minus strand of HIV-1 DNA, resulting in G to A hypermutation in the plus strand of DNA. Thus, APOBEC3G and APOBEC3F provide a mechanism for innate immunity to retroviruses, and are also likely contribute to sequence variation observed in many viruses. Viral infectivity factor (Vif) imparts APOBEC3G and APOBEC3F resistance to HIV through impaired translation of their mRNA and accelerated posttranslational degradation of the APOBEC3 proteins by the 26S proteasome. Interestingly, HIV-1 Vif cannot form a complex with APOBEC3G or APOBEC3F of mouse origin as it does with the human protein, and thus mouse APOBEC3G and APOBEC3F function as a potent inhibitors of wildtype HIV-1 replication, where human APOBEC3G and APOBEC3F are only able to inhibit Vif-deficient HIV-1 replication. This implies that induction of APOBEC3G and APOBEC3F activity or a method of blocking their interaction with Vif may provide a method for therapeutic intervention.
UOM:
1 * 100 µl
Fournisseur:
LIOFILCHEM S.R.L.
Description:
Lyophilised reference stock culture preparations containing a single strain of a microorganism for quality control of culture media, education and proficiency programs. Lyophilisation is a method for long-term preservation of microorganisms. The microorganism preparations are derived from NCTC® (National Collection of Type Cultures by the UK Health Security Agency - UKHSA).
Numéro de catalogue:
(PRLS90341.290)
Fournisseur:
PROLABO CMP
Description:
In accordance with the operating mode: 50 mg SODIUM PENTACYANONITROSYLFERRATE 2H2O ANALAR Ref VWR 27966 10 g PHENOL FOR ACS ANALYSES Ref Merck 100206 QSP 1000 ml deionised water.
UOM:
1 * 1 L
New Product
Numéro de catalogue:
(BOSSBS-11889R-A647)
Fournisseur:
Bioss
Description:
Hox, Pbx and Meis families of transcription factors form heteromeric complexes and bind DNA through specific homeobox domains. Hox proteins are involved in regulating tissue patterning during development, and are also expressed in lineage- and stage-specific patterns during adult hematopoietic differentiation and in leukemias. The Hox proteins, which include paralog groups 1-10, have a low intrinsic binding affinity for DNA and are instead associated into cooperative DNA binding complexes with Pbx or the Pbx- related Meis proteins, which result in an enhanced Hox-DNA binding affinity and an increased selectivity for the binding site. Both Meis1 and Meis2 (also known as Meis-related gene 1 or Mrg1) are members of the TALE (“three amino acid loop extensionâ€) family of homeodomain-containing proteins. In addition to binding with Hox proteins, Meis1 also forms heterodimers with the ubiquitously expressed Pbx proteins, including Pbx1, Pbx2 and Pbx3, and these complexes contain distinct DNA-binding specificities. Like Hox and Pbx proteins, Meis1 is implicated in oncogenesis, as it is overexpressed as a result of adjacent retroviral insertion in BHX-2 myeloid leukemias. Two Meis-related proteins, Meis2 and Meis3 (also designated Mrg1 and Mrg2, respectively), possess largely similar sequence identity with Meis1 and are expressed in normal tissues and myeloid leukemias. In the pancreas, Meis2 preferentially associates with Pbx1, and together they associate with the pancreas-specific homeodomain factor, Pdx1, to repress Pdx1-induced transcriptional activation.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0170R-A680)
Fournisseur:
Bioss
Description:
Tyrosine-protein kinase that acts as a cell-surface receptor for VEGFA, VEGFB and PGF, and plays an essential role in the development of embryonic vasculature, the regulation of angiogenesis, cell survival, cell migration, macrophage function, chemotaxis, and cancer cell invasion. May play an essential role as a negative regulator of embryonic angiogenesis by inhibiting excessive proliferation of endothelial cells. Can promote endothelial cell proliferation, survival and angiogenesis in adulthood. Its function in promoting cell proliferation seems to be cell-type specific. Promotes PGF-mediated proliferation of endothelial cells, and proliferation of some types of cancer cells, but does not promote proliferation of normal fibroblasts. Has very high affinity for VEGFA and relatively low protein kinase activity; may function as a negative regulator of VEGFA signaling by limiting the amount of free VEGFA and preventing its binding to KDR. Modulates KDR signaling by forming heterodimers with KDR. Ligand binding leads to the activation of several signaling cascades. Activation of PLCG leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate and the activation of protein kinase C. Mediates phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, leading to the activation of phosphatidylinositol kinase and the downstream signaling pathway. Mediates activation of MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. Phosphorylates SRC, YES1 and PLCG, and may also phosphorylate CBL. Promotes phosphorylation of AKT1 and PTK2/FAK1 (By similarity).
UOM:
1 * 100 µl
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