C1q, the first component of the classical pathway of the complement system, interacts with various cell types and triggers a variety of cell-specific cellular responses, such as oxidative burst, chemotaxis, phagocytosis, etc. Different biological responses are attributed to the interaction of C1q with more than one putative cell-surface C1q receptor/C1q-binding protein. Previously, it has been shown that C1q-mediated oxidative burst by neutrophils is not linked to G-protein-coupled fMet-Leu-Phe-mediated response. In the present study, we have investigated neutrophil migration brought about by C1q and tried to identify the signal-transduction pathways involved in the chemotactic response. We found that C1q stimulated neutrophil migration in a dose-dependent manner, primarily by enhancing chemotaxis (directed movement) rather than chemokinesis (random movement). This C1q-induced chemotaxis could be abolished by an inhibitor of G-proteins (pertussis toxin) and PtdIns(3,4,5)P3 kinase (wortmannin and ...
Abstract: Recent studies have focused on elucidating the contribution of individual complement proteins to post-ischemic cellular injury. As the timing of complement activation and deposition after cerebral ischemia is not well understood, our study investigates the temporal pattern of C1q accumulation after experimental murine stroke. Brains were harvested from mice subjected to transient focal cerebral ischemia at 3, 6, 12, and 24 hr post reperfusion. Western blotting and light microscopy were employed to determine the temporal course of C1q protein accumulation and correlate this sequence with infarct evolution observed with TTC staining. Confocal microscopy was utilized to further characterize the cellular localization and characteristics of C1q deposition. Western Blot analysis showed that C1q protein begins to accumulate in the ischemic hemisphere between 3 and 6 hr post-ischemia. Light microscopy confirmed these findings, showing concurrent C1q protein staining of neurons. Confocal ...
The invention provides a series of G.alpha..sub.q protein variants that functionally couple to sensory cell receptors such as taste GPCRs (TRs) and olfactory GPCRs (ORs) in an overly promiscuous manner. According to the invention, the functional coupling can be determined, for example, by measuring changes in intracellular IP3, or calcium. In a particular embodiment, the G.alpha..sub.q protein variants can be expressed in mammalian cell lines or Xenopus oocytes, and then evaluated using calcium fluorescence imaging and electrophysiological recording.
Influence of the Gαq-protein on myocardial infarct size of the bone marrow-engrafted Gαq-knockout-mouse in a ischemia/reperfusion-model Platelets play a key role in the pathogenesis of an acute myocardial infarction. Thrombus formation, which is mediated by the activation of platelets, results in the occlusion of the coronary artery. On the other hand, agglutinated platelets in the small myocardial vessels impair the myocardial microcirculation. Due to their pro-inflammatory effects, platelets also contribute to the pathogenesis of ischemia/reperfusion injury. The myocardium of Gαq-deficient mice showed a reduced susceptibility to ischemia and reperfusion compared to that of wild-type mice (HEUER, in preparation). Activation of platelets lacking the Gαq-protein is markedly impaired, resulting not only in an increased haemophilia but also in a decreased thrombophilia of Gαq-deficient mice. A bone marrow transplantation was performed to investigate whether the impaired platelet-activation is ...
In a previous study we isolated a series of rat monoclonal antibodies to the human leukocyte common (LC) antigen and demonstrated that synergistic complement lysis was possible between IgG2b antibodies which recognised different epitopes. In this report we have examined the mechanisms that were involved in synergistic lysis. We found that the number of C1q binding sites increased from 30,000 to 40,000/cell using a single antibody to 90,000/cell when two IgG2b antibodies to different epitopes were used together. The affinity of C1q binding also increased approx. 3-fold for the synergistic pair, and there was a similar increase in the rate of C1 activation. Combinations of an IgG2b with IgG1 or IgG2a gave much smaller increases in the amount of C1q bound and in the rate of C1 activation. Despite the large number of C1q molecules bound with the optimal synergistic pair and the increased rate of C1 activation, lysis was inefficient in serum depleted of Factor D, suggesting a requirement for the alternative
Combining with the C1q component of the classical complement cascade and transmitting the signal from one side of the membrane to the other to initiate a change in cell activity.
In addition to binding to cadherins, Gα12 and Gα13 were found to play important roles in other adhesion molecule-dependent cellular functions. In platelets lacking Gαq, coactivation of the Gαq- and Gα12/13-coupled thromboxane A2 receptor and the Gαi-coupled ADP receptor P2Y12 resulted in irreversible integrin αIIbβ3-mediated platelet aggregation (Nieswandt et al., 2002). Because Gαq-deficient platelets fail to respond to thromboxane A2 in αIIbβ3 activation assay, the study demonstrates converging signaling of Gα12/13 and Gαi, which is sufficient to overcome Gαq deficiency for αIIbβ3 activation. A recent study provided evidence for a role of the G12 subfamily in integrin signaling by demonstrating a direct interaction of Gα13 with the cytoplasmic domain of the β3 integrin (Gong et al., 2010). Ligand binding to the integrin αIIbβ3, as well as GTP loading of Gα13, promotes this interaction, supporting an "outside-in" signaling mechanism that favors cell spreading through the ...
* found in: Quartz (particle size), SIGMA Quercetin-3-D-xyloside |=97.0% (HPLC), Quercetin =95% (HPLC), solid, QuadraPure™ TU, 400-600 micron, metal..
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Complete information for MIR548Q gene (RNA Gene), MicroRNA 548q, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
It has been suggested that the human C1qRp is a receptor for the complement component C1q; however, there is no direct evidence for an interaction between C1q and C1qRp. In this study, we demonstrate that C1q does not show enhanced binding to C1qRp-transfected cells compared with control cells. Furthermore, a soluble recombinant C1qRp-Fc chimera failed to interact with immobilized C1q. The proposed role of C1qRp in the phagocytic response in vivo is also unsupported in that we demonstrate that this molecule is not expressed by macrophages in a variety of human tissues and the predominant site of expression is on endothelial cells. Studies on the rodent homolog of C1qRp, known as AA4, have suggested that this molecule may function as an intercellular adhesion molecule. Here we show that C1qRp is the Ag recognized by several previously described mAbs, mNI-11 and two anti-CD93 Abs (clones X2 and VIMD2b). Interestingly, mNI-11 (Fab) has been shown to promote monocyte-monocyte and ...
Molecular, biochemical and functional characterizations of C1q/TNF family members: adipose-tissue-selective expression patterns, regulation by PPAR-gamma agonist, cysteine-mediated oligomerizations, combinatorial associations and metabolic functions ...
Lamont & Tonelli talked to Mr. Skin for his weekly fun bags forecast, including the return of "The L Word: Generation Q" on Showtime, a nude photo of Amy Schumer on her Instagram. Plus, Jennifer Lopez and Lizzo wearing thongs in their movie "Hustlers.". ...
ASSIGNMENT STATEMENTS * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1762:E10b] IS (3) OR ([Q1763:E10c] IS (1 OR DK OR RF) AND [Q1762:E10b] IS (A)) OR [Q1765:E10Y1b1] IS (3 OR 5) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1767] IS (3 OR 5) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1760:E10] IS (A) AND [Q1760:E10] IS (NE DK AND NE RF) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1766] IS (3 OR 5) OR ([Q1761:E10a] IS (3) OR ([Q1762:E10b] IS (1 OR DK OR RF) AND [Q1761:E10a] IS (A))) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1764:E10b1] IS (3 OR 5) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1763:E10c] IS (3) OR [Q1764:E10b1] IS (1 OR DK OR RF) * Jump from R1842 [E24Y1.ASSIGN NH/HOSP $] when [Q1:PR1] IS (GE 0 OR LE 0) * if [Q1800] IS (A) AND [Q1800] IS (NE DK AND NE RF) then [R1843.E24Y2.ASSIGN DR/OUTPATIENT $] = system calculation: 1800 * if [Q1804] IS (3 OR 5) then [R1843.E24Y2.ASSIGN DR/OUTPATIENT $] = 20000 * if [Q1803] IS (3) OR [Q1804] IS (1 OR DK OR RF) ...
XY, +20, dup(1)(q21q42), der(2)t(2;14)(q37;q24)t(14;18)(q32;q21), t(8;22)(q24;q11.2), der(14)t(X;14)(p21;p13)t(14;18)(q32;q21), dup(17)(q11q22), der(18)t(14;18)(q32;q21); ...
C5b-9小鼠单克隆抗体[aE11](ab66768)可与马, 人, 猪, 猴, 狒狒样本反应并经ELISA, IHC, Flow Cyt, ICC/IF实验严格验证,被7篇文献引用并得到1个独立的用户反馈。
C9小鼠单克隆抗体[aE11](ab90801)可与马, 人, 猪样本反应并经ELISA, IHC, FuncS, Flow Cyt实验严格验证,被5篇文献引用。所有产品均提供质保服务,中国75%以上现货。
NUMBER OF TESTS TAKEN: 210 (no excused absences) Q2Q1 Q2Q2 Q2Q3 Q2Q4 Quiz2 AVERAGE 9.8 7.6 8.9 10.5 36.8 STDEV 2.9 3.2 1.5 2.9 7.3 AVEDEV 2.3 2.6 1.2 2.2 5.9 MINIMUM 1.0 0.0 2.0 2.5 13.0 MAXIMUM 15.0 10.0 10.0 15.0 49.0 Max. Possible 10.0 10.0 10.0 10.0 50.0 ...
XY, +5, +5, +6, -8, +mar, der(5)t(5;6)(q35;p21), t(5;6)(q35;p21), add(10)(q23-24), der(13)t(1;13)(q32;p11)t(1;13)(q21;q34), add(16)(q23), add(19)(p13), 33% - 74(74- ...
All your questions about OldPain2Go answered in this Q and A. Q. Does it work? A. A. Yes it can with a client who is positively wanting to be pain-free.
过了due date宝宝依然没有出动的样子。 爷爷奶奶也因签证到期不得不回国了。 遗憾没能见到小孙女。. 最后一两周Q小某天天在我耳边叨叨让我多走路,帮助顺产。 我也尽力走啊~ 那时候真的走一会就累得想坐下休息。 生前的一晚Q小某还对肚子说,Charlotte你快出来吧。你如果今晚出动,等你一岁生日时爸爸给你买个大hello kitty猫。 结果Charlotte还真听话。 清晨太阳还没升起时,我在睡梦中忽然感觉水破了。 我也没有洗澡,叫Q小某起床准备去医院。我父母刚好在,也马上起来给我做了碗面汤,急急忙忙吃后我和Q小某就去医院了。 7AM左右就到了医院。 就不细写产经了。总而言之,催产催不出来,下午五点就刨了(5:15pm 宝宝的出生时间,to be exact)。 ...
/PRNewswire/ -- HubSpot, Inc. (NYSE: HUBS), a leading growth platform, today announced financial results for the second quarter ended June 30, 2020. Financial...
Dietary Supplement Sugar, Salt and Starch Free Vision Support Supplement Facts Serving Size 1 Tablet Amount Per Serving - % Daily Value VitaminA (asretinolpalmitate) 5000 IU 100% VitaminC (asL-ascorbicacid) 10 mg 17% Calcium (asdicalciumphosphate) 55 mg 6% Other Ingredients: Dicalcium Phosphate, Microcrystalline Cellulose, Silica, Vegetable Cellulose, Vegetable Magnesium Stearate. IMPORTANT INFORMATION: Long term intake of high levels of Vitamin A (excluding that sourced from beta-carotene) may increase the risk of osteoporosis in postmenopausal women. Do not take this product if taking other Vitamin A (retinol form) supplements. Not for chronic use. Not formulated for use in children. If you are pregnant, nursing, taking any medication or have a medical condition, please consult your medical practitioner before taking any dietary supplement. Solgars Dry Vitamin A Tablets
In invertebrates, the medicinal leech is considered to be an interesting and appropriate model to study neuroimmune mechanisms. Indeed, this non-vertebrate animal can restore normal function of its central nervous system (CNS) after injury. Microglia accumulation at the damage site has been shown to be required for axon sprouting and for efficient regeneration. We characterized HmC1q as a novel chemotactic factor for leech microglial cell recruitment. In mammals, a C1q-binding protein (C1qBP alias gC1qR), which interacts with the globular head of C1q, has been reported to participate in C1q-mediated chemotaxis of blood immune cells. In this study, we evaluated the chemotactic activities of a recombinant form of HmC1q and its interaction with a newly characterized leech C1qBP that acts as its potential ligand. Recombinant HmC1q (rHmC1q) was produced in the yeast Pichia pastoris. Chemotaxis assays were performed to investigate rHmC1q-dependent microglia migration. The involvement of a C1qBP-related
Results Anti-C1q antibodies were more prevalent than anti-ds DNA (n=41,93.2%)in pSLE patients of the current study, which correlated significantly with proteinuria and decreased complement levels (p,0.05). Anti-C1q levels were significantly elevated in patients with class III/IV nephritis compared II/V nephritis. pSLE patients with active nephritis at the time of sample collection demonstrated significantly elevated levels of anti-C1q antibodies compared to those without active nephritis. Anti-C1q antibodies were more sensitive and specific than anti-dsDNA in pSLE patients ...
Highlights: • A human monoclonal antibody against influenza virus was produced from a volunteer. • The antibody was generated from the PBMCs of the volunteer using the fusion method. • The antibody neutralized heterosubtypically group 1 influenza A viruses (H1 and H9). • The antibody targeted a novel epitope in globular head region of the hemagglutinin. • Sequences of the identified epitope are highly conserved among H1 and H9 subtypes. - Abstract: Most neutralizing antibodies elicited during influenza virus infection or by vaccination have a narrow spectrum because they usually target variable epitopes in the globular head region of hemagglutinin (HA). In this study, we describe a human monoclonal antibody (HuMAb), 5D7, that was prepared from the peripheral blood lymphocytes of a vaccinated volunteer using the fusion method. The HuMAb heterosubtypically neutralizes group 1 influenza A viruses, including seasonal H1N1, 2009 pandemic H1N1 (H1N1pdm) and avian H9N2, with a strong ...
Background: The C3bot1 protein (~23 kDa) from Clostridium botulinum ADP-ribosylates and thereby inactivates Rho. C3bot1 is selectively taken up into the cytosol of monocytes/macrophages but not of other cell types such as epithelial cells or fibroblasts. Most likely, the internalization occurs by a specific endocytotic pathway via acidified endosomes. Methodology/Principal Findings: Here, we tested whether enzymatic inactive C3bot1E174Q serves as a macrophage-selective transport system for delivery of enzymatic active proteins into the cytosol of such cells. Having confirmed that C3bot1E174Q does not induce macrophage activation, we used the actin ADP-ribosylating C2I (~50 kDa) from Clostridium botulinum as a reporter enzyme for C3bot1E174Q-mediated delivery into macrophages. The recombinant C3bot1E174Q-C2I fusion toxin was cloned and expressed as GST-protein in Escherichia coli. Purified C3bot1E174Q-C2I was recognized by antibodies against C2I and C3bot and showed C2I-specific enzyme activity ...
We are interested in interactions between the two fundamental cell types of the nervous system, neurons and glia. My laboratory seeks to understand how neuron-glia communication facilitates the formation, elimination and plasticity of synapses-the points of communication between neurons-during both healthy development and disease.. We focus on the role of neuron-glia and neural-immune interactions in the patterning of neural circuits. We and our collaborators have identified an unexpected role for glia and components of the innate immune system in synaptic pruning. We find that astrocytes induce neuronal expression of complement C1q, the initiating protein of the classical complement cascade (which tags unwanted cells and debris for elimination in the immune system). C1q and downstream complement proteins target synapses and are required for synapse elimination in the developing visual system. Importantly, we find that C1q becomes aberrantly upregulated and is relocalized to synapses in the ...
To evaluate whether ischemic myocardium releases molecules that react with the first component of complement, we studied cardiac lymph from eight dogs before and at intervals after coronary artery occlusion and reperfusion. Before occlusion, the dogs were injected intravenously with radiolabeled human C1q. Labeled C1q could be detected in the cardiac lymph within minutes following injection. Rabbit antisera, prepared against substances precipitated from postreprefusion cardiac lymph by anti-human C1q, also reacted with specific constituents of isolated cardiac sarcoplasmic reticulum and mitochondria. To evaluate whether mitochondria are the source of these C1q-binding proteins, we isolated intramyofibrillar and subsarcolemmal mitochondria from canine heart and incubated sonicates of these with purified C1q, immobilized on nitrocellulose. Molecules bound to the immobilized C1q were removed with 0.1% sodium dodecyl sulfate, fractionated under reducing conditions by polyacrylamide gel ...
The C-reactive protein (CRP) is a cyclic pentameric pentraxin family acute phase protein compound of five identical noncovalently bound nonglycosylated subunits (each subunit 24 kDa; physiologic CRP molecule 117,5 kDa). CRP is produced by the liver and its plasma levels rise dramatically during inflammatory processes occuring in the body. CRP is an initiator of classical complement cascade, binds to several nuclear components (chromatin, histones, etc.) and is also believed to play an important role in innate immunity. Patients with elevated basal levels of CRP are at increased risk for hypertension and cardiovascular disease ...
Previous studies have shown that complement opsonization is required for efficient phagocytosis of dying cells in vitro (6, 7) and that uptake of these opsonized cells is associated with expression of the antiinflammatory cytokine, TGF-β (6). Three observations, namely that C1q binds to apoptotic cells in vitro (10), that apoptotic cells accumulate in the kidneys of mice deficient in C1q (4), and that complement activation on apoptotic cells promotes phagocytosis of these cells by macrophages in vitro, suggest a pivotal role for complement in noninflammatory clearance of dying cells. Here, we report that IgM antibodies in normal individuals are quantitatively most important for C1q binding and C3b/bi activation on the apoptotic cell surface and that these natural antibodies bind to lysophosphorylcholine that is exposed on cells undergoing apoptosis.. Since IgM bound to apoptotic cells by the Fab, rather than the Fc, portion of the Ig, binding could be attributed to antibody recognition of an ...
TY - JOUR. T1 - The mouse C1q genes are clustered on chromosome 4 and show conservation of gene organization. AU - Petry, F. AU - McClive, PJ. AU - Botto, M. AU - Morley, Bernard J. AU - Morahan, G. AU - Loos, M. PY - 1996/4. Y1 - 1996/4. N2 - Mouse complement component C1q is a serum glycoprotein which consists of six A chains, six B chains and six C chains. The three polypeptides are 223, 228, and 217 residues long, respectively, and are encoded by three genes. DNA probes for mouse C1q A, B, and C chains were hybridized to Southern blots of DNA obtained from various inbred mouse strains. On the basis of fragment length polymorphisms, two different alleles of each of the genes could be identified. The distribution of these alleles was determined in the BXD and LXPL recombinant inbred strain series. Comparison with previously reported strain distribution patterns shows that the genes encoding mouse C1q map to the same locus on distal chromosome 4. Overlapping clones spanning the entire gene ...
Most successful vaccines elicit neutralizing antibodies and this property is a high priority when developing an HIV vaccine. Indeed, passively administered neutralizing antibodies have been shown to protect against HIV challenge in some of the best available animal models. For example, antibodies gi …
Data_Sheet_1_Characterization of the C1q-Binding Ability and the IgG1-4 Subclass Profile of Preformed Anti-HLA Antibodies by Solid-Phase Assays.docx
KUALA LUMPUR (Aug 30): DutaLand Bhd returned to the black in the fourth quarter ended June 30, 2017 (4QFY17) with a net profit of RM15.08 million vers...
effect. Instead of specifying gamma directly, we select two quantities that are more intuitive and together define gamma. The first is theta, a threshold value that defines a high-impact mutation . The second is q, the fraction of mutations that exceed this threshold in their effect. For example, a user can first define a high-impact mutation as one that results in 10% or more change in fitness (theta = 0.1) relative to the scale factor and then specify that 0.001 of all mutations (q = 0.001) be in this category. Inside the code the value of is computed that satisfies these requirements. We reiterate that Mendel uses the same value for gamma, and thus the same values for theta and q, for both favorable and deleterious mutations. Figure 3.1 shows the effect of the parameter q on the shape of the distribution of fitness effect. Note that for each of the cases displayed the large majority of mutations are nearly neutral, that is, they have very small effects. Since a utation s effect on fitness can ...
Kur një rrëfim na merr me vete, përvetësojmë identitetin e personazhit dhe e stimulojmë përvojën e tij në jetën reale Shumë shpesh na ndodh që gjatë leximit të një libri, të apasionohemi aq shumë pas historisë, sa të fillojmë të identifikohemi me protagonistin e saj duke kërkuar pika të përbashkëta me të ose të kopjojmë sjelljen dhe mendimet e tij. Sipas një studimi të Universitetit shtetëror të Ohajos, ky është një proces shumë normal që studiuesit e kanë quajtur "përvetësimi i përvojës", ose procesi spontan që çon në përvetësimin e identitetit të një personazhi në një rrëfim të shkruar në një libër dhe më pas stimulimi i përvojës së tij në jetën reale. Pra, në një farë mënyrë, jeni duke humbur brenda historisë së shkruar (në mënyrë letrare) dhe e gjeni veten si pa kuptuar duke vepruar dhe menduar njësoj si protagonisti i romanit, për të arritur deri atje sa të modifikoni sjelljen tuaj në mënyrë që të jetë e ...
I regularly use resource Q on FPLC and the loaded protein always has imidazole. In fact I plan to hook up an anion exchange column in series with the Ni-NTA column and do both the purifications together to save time ...
Complete information for C1QBPP3 gene (Pseudogene), Complement C1q Binding Protein Pseudogene 3, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
46,Y,t(X;14;7)(q11;p11;q?21),t(1;8)(q21;p21),t(2;20)(p13;q13),t(5;16) (p13;q12),der(15)t(15;18)(q15;p11),der(17)t(17;18)(q23;q21),der(18)t (15;18)t(17;18)/46,Y,t(X;10)(p22;q21),t(2;5)(p23;q11),t(6;12)(q23;q21)/46, XY,der(1)t(1;17)(p31;q11)del(1)(q23),dup(1)(q21q?41),?add(6)(q25),t(7;8) (p11;q24),t(10;11)(p11;q23),?t(11;18)(p14;p11),?t(13;16)(q32;q22),t(14;22) (q22;q11),der(17)t(1;17)(p31;q11)/46,XY,inv(6)(p11p21),t(14;15)(p11;q22), inv(17)(q11q25)/46,XY,t(1;3)(q21;p21),t(1;5;13)(q21;q22;q22),t(2;16) (p13;q13),t(11;18)(q21;q21),del(15)(q24 ...
RS6B_SCHPO (Q9C0Z7 ), RS6B_YEAST (P0CX38 ), RS6E_AERPE (Q9Y9B6 ), RS6E_ARCFU (O29739 ), RS6E_CALMQ (A8MA52 ), RS6E_HALLT (B9LR51 ), RS6E_HALMA (P21509 ), RS6E_HALS3 (B0R815 ), RS6E_HALSA (Q9HMJ5 ), RS6E_HALWD (Q18DP5 ), RS6E_HYPBU (A2BJZ7 ), RS6E_METAC (Q8TQL4 ), RS6E_METAR (Q0W8B4 ), RS6E_METBF (Q466D6 ), RS6E_METBU (Q12Z92 ), RS6E_METJA (P54067 ), RS6E_METKA (Q8TVE6 ), RS6E_METMA (Q8PU79 ), RS6E_METS5 (A4YIY0 ), RS6E_METST (Q2NGM7 ), RS6E_METTH (O26360 ), RS6E_NANEQ (Q74MJ5 ), RS6E_NATPD (Q3ISW0 ), RS6E_NITMS (A9A110 ), RS6E_PYRAB (Q9UYS3 ), RS6E_PYRAE (Q8ZX25 ), RS6E_PYRAR (A4WIK0 ), RS6E_PYRCJ (A3MUD0 ), RS6E_PYRFU (Q8U3H8 ), RS6E_PYRHO (O58349 ), RS6E_PYRIL (A1RUW1 ), RS6E_PYRNV (B1YCP4 ), RS6E_STAMF (A3DMS1 ), RS6E_SULIA (C3MZ52 ), RS6E_SULIK (C4KID0 ), RS6E_SULIL (C3MR04 ), RS6E_SULIM (C3MWZ2 ), RS6E_SULIY (C3N772 ), RS6E_SULSO (Q980A6 ), RS6E_SULTO (Q975N7 ), RS6E_THEKO (Q5JDK8 ), RS6E_THEON (B6YW70 ), RS6E_THESM (C6A2D7 ), RS6_AEDAE (Q9U761 ), RS6_AEDAL (Q9U762 ), RS6_APLCA (Q9BMX5 ), ...
GLHA2_ONCKE (P69063 ), GLHA2_ONCTS (P69062 ), GLHA_ACALA (P30970 ), GLHA_AILFU (Q8HZS0 ), GLHA_AILME (Q8WN20 ), GLHA_ANGAN (P27794 ), GLHA_AOTNA (Q3HRV5 ), GLHA_BALAC (P37036 ), GLHA_BOSMU (Q19PY8 ), GLHA_BOVIN (P01217 ), GLHA_BUBBU (Q9GL36 ), GLHA_CALJA (P51499 ), GLHA_CANLF (Q9XSW8 ), GLHA_CAPHI (Q8WMW8 ), GLHA_CAVPO (Q9JK68 ), GLHA_CERNI (Q8WMR3 ), GLHA_CLAGA (P53542 ), GLHA_COTJA (P68242 ), GLHA_CTEID (P30983 ), GLHA_EQUAS (Q28365 ), GLHA_EQUBU (O46642 ), GLHA_FELCA (Q52R91 ), GLHA_FUNHE (P47744 ), GLHA_HORSE (P01220 ), GLHA_HUMAN (P01215 ), GLHA_HYPMO (P37037 ), GLHA_ICTPU (Q9YGP3 ), GLHA_LITCT (P80051 ), GLHA_MACFA (Q9BEH3 ), GLHA_MACMU (P22762 ), GLHA_MACRU (P68267 ), GLHA_MASCO (Q9ERG4 ), GLHA_MELGA (P68241 ), GLHA_MERUN (Q9ERJ6 ), GLHA_MESAU (Q9ERG5 ), GLHA_MICMO (Q9ERG3 ), GLHA_MONDO (Q6YNX4 ), GLHA_MORSA (Q91119 ), GLHA_MOUSE (P01216 ), GLHA_MURCI (P12836 ), GLHA_NIPNI (Q8JIE9 ), GLHA_PANTA (Q9BDI8 ), GLHA_PHYCD (P25329 ), GLHA_PIG (P01219 ), GLHA_RABIT (P07474 ), GLHA_RAT (P11962 ), ...
chains in the Genus database with same CATH superfamily 1N61 C; 2Q85 A; 4O95 A; 3EUB 3; 2GQU A; 1HSK A; 1QLT A; 3C0P A; 1AHZ A; 1AHV A; 2BVF A; 2VFU A; 1DIQ A; 4OAL A; 3S1C A; 1N62 C; 5FXE A; 4ML8 A; 4XLO A; 4PYT A; 3S1F A; 3TX1 A; 3S1E A; 4BC7 A; 3HRD C; 4HG0 A; 4PWB A; 1DII A; 2O3G A; 1QLU A; 4BBY A; 2W55 A; 5HQX A; 5FXP A; 2P4P A; 1WYG A; 1ZR6 A; 2MBR A; 4BCA A; 2OAI A; 1W1O A; 1FO4 A; 4UD8 A; 2NQW A; 1N63 C; 2VAO A; 3NRZ B; 3LAE A; 4BC9 A; 3FWA A; 1W1S A; 1V97 A; 2QPM A; 2VFS A; 3BW7 A; 3TSH A; 3NVW B; 4PVH A; 2BVH A; 4PVE A; 2VFR A; 1T3Q C; 1W1Q A; 3FW9 A; 3I99 A; 1E8G A; 2RK5 A; 1N5X A; 1JRO A; 2PLS A; 1E0Y A; 1I19 A; 3B9J B; 3PM9 A; 4PZF A; 1AHU A; 1N60 C; 1UXY A; 4JB1 A; 2E3T A; 4ZOH B; 5AE3 A; 5AE2 A; 3FW8 A; 2P3H A; 3GSY A; 5HMR A; 3TSJ A; 5D79 A; 5G5H B; 3W8X A; 3D2D A; 1W1R A; 1N5W C; 1E8H A; 3DED A; 3AN1 A; 2W54 A; 2EXR A; 2I0K A; 5G5G B; 2R8D A; 5HHZ A; 1ZXI C; 3W8W A; 3DQ0 A; 4PVJ A; 1F0X A; 1E8F A; 2W3S A; 1MBT A; 3SR6 B; 1RM6 B; 1VAO A; 3ETR B; 5FXD A; 2VFT A; 3D2J A; 1WVE A; ...
マウス・モノクローナル抗体 ab17931 交差種: Hu 適用: WB,ELISA,IHC-P,Flow Cyt…C9抗体一覧…画像、プロトコール、文献などWeb上の情報が満載のアブカムの Antibody 製品。国内在庫と品質保証制度も充実。
D123E, I135T, R172RK, I178M, E204Q, Q207E, R211K, F214L, V245Q, E248D, A272P, T286V, E291D, I293V, E297V, A327V, Q394L, A400T, E404D, K431T, V435A, A446S, L452K, V466A, V467I, D471E, T477A, H483Q, L491S, E492D, K512Q, S519N, ...
K20R, V35I, E44G, S48F, D123S, K173A, Q174E, I178L, Q207E, E233X, V245Q, E248D, D250E, S251A, A272P, K275Q, T286A, V292I, E297A, L303M, P321S, S322A, D324E, I329V, Q334L, G335D, R356K, M357R, G359S, A360T, T369A, A371V, T377L, F389I, K390R, A400T, E404D, L422M, E432D, V435A, R461K, D471E, Q480H, L491S, S519N, K530R, A534S, A554N ...
Q. Im like Mark Twains quote: Quitting smoking is easy; Ive done it a thousand times. Now, I really would like to quit. Got any suggestions?A. Twain may not have been truly successful in his
Complement component 1 Q subcomponent-binding protein, mitochondrial is a protein that in humans is encoded by the C1QBP gene.[5][6][7] The human complement subcomponent C1q associates with C1r and C1s in order to yield the first component of the serum complement system. The protein encoded by this gene is known to bind to the globular heads of C1q molecules and inhibit C1 activation. This protein has also been identified as the p32 subunit of pre-mRNA splicing factor SF2, as well as a hyaluronic acid-binding protein.[7] ...
Microglia, central nervous system (CNS) resident phagocytic cells, persistently police the integrity of CNS tissue and respond to any kind of damage or pathophysiological changes. These cells sense and rapidly respond to danger and inflammatory signals by changing their cell morphology; by release of cytokines, chemokines, or nitric oxide; and by changing their MHC expression profile. We have shown previously that microglial biosynthesis of the complement subcomponent C1q may serve as a reliable marker of microglial activation ranging from undetectable levels of C1q biosynthesis in resting microglia to abundant C1q expression in activated, nonramified microglia. In this study, we demonstrate that cultured microglial cells respond to extrinsic C1q with a marked intracellular Ca2+ increase. A shift toward proinflammatory microglial activation is indicated by the release of interleukin-6, tumor necrosis factor-alpha, and nitric oxide and the oxidative burst in rat primary microglial cells, an ...
Here, we have addressed the role of an impairment of H2S oxidation in the pathogenesis of CoQ deficiency. We demonstrated that CoQ‐deficient fibroblasts carrying mutations in different COQ genes have decreased SQR‐driven respiration, which is associated with variably reduced SQR steady‐state levels, depending on the severity of CoQ deficiency, and subsequent compensatory up‐regulation of the levels of the downstream proteins of the pathway. We hypothesize that if the levels of CoQ are very low, SQR activity is decreased and SQR becomes unstable and is probably degraded. Partial reduction in SQR and/or its activity leads to up‐regulation of the enzymes of the downstream pathway (TST, ETHE1, and SUOX), which is more evident at the translational than at transcriptional level. The molecular abnormalities observed in COQ‐mutant fibroblasts are due to reduced CoQ levels, because they can be rescued by CoQ supplementation and are partially recapitulated by pharmacological inhibition of CoQ ...