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1 ntains ancient mitochondrial DNA of a modern human type.
2 composed of the extracellular portion of the human type 1 (p55) tumor necrosis factor receptor (TNFR)
6 r understanding of the structure/function of human type 1 and 2 3beta-HSD/isomerase may lead to the d
7 six sulfonamide inhibitors to two isozymes (human type 1 and bovine type 2) was analyzed by both The
18 of PTPN22 as a novel susceptibility gene in human type 1 diabetes and continued progress in defining
20 tivator of transcription (STAT) 1 pathway in human type 1 diabetes and in mouse models, especially in
22 r response to the (B9-23) insulin epitope in human type 1 diabetes and suggests that the mouse and hu
23 may be an antigen for pathogenic T cells in human type 1 diabetes and, thus, a new, potential target
24 imal models is well-established, but data on human type 1 diabetes are tentative and based on studies
25 es with NOD mice, increased understanding of human type 1 diabetes can be gained by evaluating the pa
29 ne diabetes to provide valuable insights for human type 1 diabetes in terms of pancreatic histopathol
32 immune insulin-dependent diabetes similar to human type 1 diabetes mellitus (T1DM), whereas the BBDR+
33 ed cellular and molecular phenotyping of the human type 1 diabetes pancreas is lacking, limiting our
34 Pancreas Analysis Program (HPAP) to procure human type 1 diabetes pancreata for an extensive array o
37 reviously utilized a novel bioassay in which human type 1 diabetes sera were used to induce a disease
39 ate of blood NK cells at different stages of human type 1 diabetes, and whether genetic or phenotypic
40 in different autoimmune diseases, including human type 1 diabetes, but their relationship to changes
42 class II gene most commonly associated with human type 1 diabetes, direct in vivo experimental evide
44 ce, the most widely studied animal model for human type 1 diabetes, failed to prevent the development
45 ecule showing the strongest association with human type 1 diabetes, in the diabetes-predisposing mili
46 ite its importance as a major autoantigen in human type 1 diabetes, it is not required for the develo
47 key determinant of genetic susceptibility to human type 1 diabetes, spontaneous diabetes has been obs
49 ing a nonobese diabetic (NOD) mouse model of human type 1 diabetes, we investigated whether tolerance
50 ese diabetic (NOD) mouse is a good model for human type 1 diabetes, which is characterized by autorea
51 (UK93) indicated a similar genetic basis for human type 1 diabetes, with the major genetic component
71 h a macrophage subpopulation in NOD mice and human type 1 diabetic samples and, hence, potentially a
72 ouses the genomic sequence data for both the human type 1 H strain and the bovine type 2 IOWA strain
73 f a novel TGF-beta-responsive element in the human type 1 plasminogen activator inhibitor promoter th
74 large N-terminal extracellular domain of the human type 1 PTH receptor (hP1Rc-WT) with residues 1-9 o
78 LC30A8) is a major target of autoimmunity in human type 1A diabetes and is implicated in type 2 diabe
81 ll interference RNA transfection of cultured human type 2 cells blocked processing of 35S-labeled pro
87 eatic duodenal homeobox (PDX1) are linked to human type 2 diabetes and maturity-onset diabetes of the
89 We focused on Spry2-a gene implicated in human type 2 diabetes by genome-wide association studies
90 tional network to induce genes identified in human type 2 diabetes genome-wide association studies li
91 A small number of susceptibility genes for human type 2 diabetes have been identified by candidate
92 pted genetically determined rodent model for human type 2 diabetes is the Goto-Kakizaki (GK) rat; how
96 of diabetes mellitus that closely resembles human type 2 diabetes, including the formation of amyloi
98 slet MMP-9 activity may also be decreased in human type 2 diabetes, thereby contributing to increased
99 n deficiency in adipocytes in mice resembles human type 2 diabetes, with early insulin resistance and
109 periments with the Tritrichomonas foetus and human type 2 IMPDHs using tiazofurin and ADP, which bind
117 n-incompetent adenoviral vector encoding the human type 2 somatostatin receptor (Ad5-CMVhSSTr2).
118 lication-incompetent adenovirus encoding the human type 2 somatostatin receptor (hSSTr2) and the herp
121 Here, we report structural findings of the human type-3 IP(3)R (IP(3)R-3) obtained by cryo-EM (at a
125 oyed the blood group A and B antigenicity of human type A and B erythrocytes, but also released A-Tri
126 ociation constant of the GS-I isolectins for human type A erythrocytes increases with increasing vale
127 ffinity displayed by the GS-I isolectins for human type A erythrocytes is dependent on their multival
128 e was present in type A strains from healthy humans, type A strains causing CPE-associated antibiotic
129 ur-coordinate cob(II)alamin, variants of the human-type ACA enzyme from L. reuteri (LrPduO) were kine
130 d the high-resolution crystal structure of a human-type ACA from Lactobacillus reuteri with a four-co
131 me promotes catalysis, several variants of a human-type ACA from the lactic acid bacterium Lactobacil
133 es exhibit a strong shift toward binding to "human-type" alpha2-6 sialosides but with notable differe
134 (9 of 9), and AB (4 of 4) RBCs; however, few human type B RBC samples (4 of 14) were hemagglutinated.
139 ASH (Drosophila, Arabidopsis, Synechocystis, Human)-type cryptochromes (cry-DASH) belong to a family
140 o acid mutations also alter binding to minor human-type glycans, suggesting that host adaptation may
143 ve tumors that correlates with expression of human type I and III IFNs derived from the cancer cells.
146 ical plasma membrane protein specific to the human type I cell, is a biochemical marker for lung inju
147 egions of different helical stability within human type I collagen and discussed their role in interm
148 , capillary-like networks by overlaying with human type I collagen followed by a second overlay of co
149 e, the more complex heterotrimeric C-telo of human type I collagen has been built from the correct se
150 mics simulations to explore the structure of human type I collagen in the vicinity of the collagenase
153 sequence for the alpha1 and alpha2 chains of human type I collagen, and the known amino acid sequence
154 s platelet-specific receptor to its ligands, human type I collagen, collagen-related peptide (CRP), a
155 8(+) T cell clone of pathogenic relevance in human type I diabetes recognizes >one million distinct d
156 e diabetic (NOD) mouse is an animal model of human type I diabetes with a strong genetic component th
158 Interestingly, the interaction between the human type I IFN receptor and STAT1 is not direct but me
160 alphas) and the extracellular (EC) domain of human type I IFN receptor subunit 2 (IFNAR2) was analyze
161 Studies have indicated that ZIKV evades the human type I IFN response, suggesting a role for the ada
164 for STAT4 recruitment and activation by the human type I IFNAR (IFN-alphabetaR), it is not sufficien
166 e I interferons (IFNs), bovine IFNAR-1 binds human Type I IFNs with moderate (nM) affinity, and can b
169 aliana) plants constitutively expressing the human type I inositol polyphosphate 5-phosphatase (InsP
170 ana tabacum) cells were transformed with the human type I inositol polyphosphate 5-phosphatase (InsP
171 show that the constitutive expression of the human type I InsP 5-ptase in tobacco cells leads to an u
175 an IFNAR-1 has a weak intrinsic affinity for human Type I interferons (IFNs), bovine IFNAR-1 binds hu
179 were engineered with a constitutively active human type I Nodal receptor (caACVR1b) to mimic activati
184 in, which associates with both SmRK1 and the human type I TGF beta receptor (T beta RI); overexpressi
187 sing simulated data for three model species: humans (type I survival), sparrow (type II), and barnacl
192 ructural and mechanistic properties with the human type IB enzyme (hTopo) and is important for viral
195 for induction of the CXC chemokine IL-8, in human type II alveolar (A549) cells by RSV infection and
196 tant demonstrated decreased adherence to the human type II alveolar cells, reduced nasopharyngeal col
198 of RSV-induced RANTES promoter activation in human type II alveolar epithelial cells (A549 cells).
199 n the induction of RANTES gene expression in human type II alveolar epithelial cells (A549), followin
201 competitive inhibition of the mitochondrial human type II arginase by N(omega)-hydroxy-L-arginine, t
203 BEC are classical, competitive inhibitors of human type II arginase with K(i) values of 0.25 and 0.31
206 with cartilage proteoglycan aggrecan (PG) or human type II collagen (CII) emulsified with Freund's co
209 the immune response to collagen, recombinant human type II collagen (rCII) was produced using a yeast
217 orated random abasic sites into plasmid DNA, human type II enzymes can locate lesions even within a b
219 od vessels and mutations of the ALK1 gene in human type II hereditary hemorrhagic telangiectasia pati
221 human IL-1alpha and IL-1beta to the soluble human type II IL-1 receptor by approximately 100-fold, w
223 up-regulated in rapidly proliferating cells, human type II IMPDH is actively targeted for immunosuppr
228 tably transfected NIH 3T3 cells expressing a human type II procollagen gene under the control of the
230 ave selectively expressed a kinase-deficient human type II TGFbeta receptor (TbetaRIIDeltak) in fibro
238 spect, we have stably overexpressed FRA-1 in human type-II-like alveolar malignant cell line (A549) a
240 ded 57 peptides derived from the sequence of human type III collagen and 9 peptides derived from the
241 olysis, varying numbers of GXY triplets from human type III collagen around the collagenase cleavage
242 model the imino acid-poor 785-796 region of human type III collagen just C-terminal to the matrix me
243 identified a high affinity binding region in human type III collagen recognized by alpha(1)I and alph
244 rminal quarter, 252 residues, of the natural human type III collagen was attached to (GPP)7 with the
245 murine leukemia virus, this receptor is the human type III sodium-dependent inorganic phosphate tran
246 tency and mechanism of block on the neuronal human type III voltage-gated sodium channel expressed in
256 ents evidence that in cells that express the human-type Na,K-ATPase, dopamine inhibits and phorbol es
257 ic acid-containing receptors, referred to as human-type (NeuAcalpha2-6Gal) and avian-type (NeuAcalpha
262 ylation pathway and can produce well defined human-type O- and N-linked glycans on recombinant therap
263 ereby accomplishes the conversion of regular human type-O blood into a potential blood substitute for
264 generation of SM6 decorated with sialylated human-type oligosaccharides, comparable to plasma-derive
266 mics in humans, maintenance and evolution of human-type receptor specificity in subsequent seasonal I
269 ombinations of the substitutions can lead to human-type receptor specificity, accumulation of multipl
270 ty but (iii) lost preferences for binding to human-type receptor while maintaining binding for the av
271 olated several mutants that maintained their human-type receptor-binding preference but acquired an a
275 the ectodomain of an H5 HA (altered to bind human-type receptors) to three rounds of treatment at 50
276 s need several adaptive mutations to bind to human-type receptors, increase hemagglutinin (HA) stabil
277 reassortant virus preferentially recognized human-type receptors, replicated efficiently in ferrets,
279 s possessing HA-222D preferentially bound to human-type receptors, while those encoding HA-222G bound
284 hemagglutinin showed stronger binding to the human-type sialic acid receptor, with preferential bindi
285 nd that H3N2 viruses have in fact maintained human-type specificity, but they have evolved preference
287 cDNA library, using the N-terminal region of human type V adenylyl cyclase (hACV) as bait, we identif
288 ics of Galpha(s) and Galpha(i) regulation of human type V and type VI adenylyl cyclase (AC V and AC V
290 displayed dipeptidase activity and degraded human type VI collagen and fibrinogen, but not salivary
296 d skin specimens showed strong expression of human type VII collagen restricted to the basement membr
297 n-collagenous amino-terminal domain (NC1) of human type VII collagen, the domain known to contain imm
298 of normal human fibroblasts can generate new human type-VII collagen and anchoring fibrils at the DEJ
300 tal structure of the trimerization domain of human type XVIII collagen, a member of the multiplexin f