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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)
3                                          The human type 1 (placenta, breast tumors, and prostate tumo
4                                              Human type 1 3 beta-hydroxysteroid dehydrogenase/isomera
5  are present in the primary structure of the human type 1 3beta-HSD/isomerase.
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
8  genetic analyses have significantly refined human type 1 diabetes (T1D) associated loci.
9 n NOD mice, evidence of their involvement in human type 1 diabetes (T1D) has been circumstantial.
10           Events defining the progression to human type 1 diabetes (T1D) have remained elusive owing
11                                              Human type 1 diabetes (T1D) is an autoimmune disease ass
12        Nonobese diabetic (NOD) mice and some human type 1 diabetes (T1D) patients manifest low to hig
13 ZnT8) is a major target of autoantibodies in human type 1 diabetes (T1D).
14  about its involvement in the development of human type 1 diabetes (T1D).
15 genic disease that resembles in many aspects human type 1 diabetes (T1D).
16 R) gene is associated with susceptibility to human type 1 diabetes (T1D).
17                               NOD mice model human type 1 diabetes and are used to investigate tolera
18  of PTPN22 as a novel susceptibility gene in human type 1 diabetes and continued progress in defining
19                         This is relevant for human type 1 diabetes and has implications for the use o
20 tivator of transcription (STAT) 1 pathway in human type 1 diabetes and in mouse models, especially in
21               CD8(+) T cells are critical in human type 1 diabetes and in the NOD mouse.
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
26                      In the current study, a human type 1 diabetes candidate region on chromosome 1q4
27                                These data in human type 1 diabetes emphasize the role of Th1/Th17 pla
28                Its involvement in murine and human type 1 diabetes has recently been recognized throu
29 ne diabetes to provide valuable insights for human type 1 diabetes in terms of pancreatic histopathol
30                                              Human type 1 diabetes is associated with defects in the
31                                              Human type 1 diabetes mellitus (T1DM) arises through aut
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
35                                           In human type 1 diabetes pancreatic islets, fasting conditi
36                          Numerous aspects of human type 1 diabetes pathogenesis are recapitulated in
37 reviously utilized a novel bioassay in which human type 1 diabetes sera were used to induce a disease
38                                     Like the human type 1 diabetes signature, the DRlyp/lyp signature
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
41                          The pathogenesis of human type 1 diabetes, characterized by immune-mediated
42  class II gene most commonly associated with human type 1 diabetes, direct in vivo experimental evide
43                 NOD mice, a model strain for human type 1 diabetes, express proinsulin (PI) in the th
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
48                              Also similar to human type 1 diabetes, the canonical canine disorder app
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
52 rediabetic NOD mice-the prototypic model for human type 1 diabetes.
53 rogressive beta-cell failure in NOD mice and human type 1 diabetes.
54 utoimmune responses in NOD mice, a model for human type 1 diabetes.
55 be a promising strategy for interventions in human type 1 diabetes.
56  dichotomy for the involvement of viruses in human type 1 diabetes.
57 and is a major autoantigen in both mouse and human type 1 diabetes.
58  great potential for immune intervention for human type 1 diabetes.
59 e of B cells in pancreatic islets as seen in human type 1 diabetes.
60 iabetes in the NOD mouse, an animal model of human type 1 diabetes.
61 al determinants of genetic susceptibility to human type 1 diabetes.
62 D) mice provides for their use as a model of human type 1 diabetes.
63 candidates for determining susceptibility to human type 1 diabetes.
64 ding T cell metabolism in the progression of human type 1 diabetes.
65 oimmunity and impaired beta cell function in human type 1 diabetes.
66 in the LEW.1AR1-iddm rat, an animal model of human type 1 diabetes.
67 L-17 on human islets have been implicated in human type 1 diabetes.
68 3 and IL-7 for the treatment of recent-onset human type 1 diabetes.
69 opment of type 1 diabetes in NOD mice and in human type 1 diabetes.
70 serpinB13 was associated with early onset of human type 1 diabetes.
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
75                          An animal model for human type 1 VWD, the RIIIS/J mouse strain, exhibits a p
76                These results suggest that in humans, type 1 responses play an important role in mucos
77 h-level IL-12p70 secretion characteristic of human type-1 polarized dendritic cells.
78 LC30A8) is a major target of autoimmunity in human type 1A diabetes and is implicated in type 2 diabe
79 n implicated in the regulation of murine and human type 1a diabetes.
80 ously reported for circulating iNKT cells in human type 1a diabetes.
81 ll interference RNA transfection of cultured human type 2 cells blocked processing of 35S-labeled pro
82 ion-PCR, both forms were detected in primary human type 2 cells.
83                                              Human type 2 cytokine responsiveness to schistosome anti
84       We performed molecular scanning of the human type 2 deiodinase (DIO2) gene and evaluated a nove
85  Islet amyloid accumulation is a hallmark of human type 2 diabetes (T2D).
86 as been implicated in the pathophysiology of human type 2 diabetes (T2DM).
87 eatic duodenal homeobox (PDX1) are linked to human type 2 diabetes and maturity-onset diabetes of the
88 ly-regulated hepatokine that is increased in human type 2 diabetes and obesity.
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
93 or have long been suggested to contribute to human type 2 diabetes mellitus.
94 d provide a unique in vitro system emulating human type 2 diabetes mellitus.
95             PPARgamma ligands, used to treat human type 2 diabetes, also down-regulate most immune sy
96  of diabetes mellitus that closely resembles human type 2 diabetes, including the formation of amyloi
97                       Obesity predisposes to human type 2 diabetes, the most common cause of diabetic
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
100 e strain BKS.Cg-m +/+ Lepr(db)/J, a model of human type 2 diabetes.
101 expression in the impaired islet function of human type 2 diabetes.
102 lar mechanisms underlying the development of human type 2 diabetes.
103  they would exhibit a phenotype more akin to human type 2 diabetes.
104 n could contribute to the islet phenotype of human type 2 diabetes.
105 ells upon diabetogenic insults, including in human type 2 diabetic islets.
106 inhibitors are virtually independent for the human type 2 enzyme.
107 eplaced by Arg and Gln, respectively, in the human type 2 enzyme.
108 7B as a novel component in the regulation of human type 2 immunity.
109 periments with the Tritrichomonas foetus and human type 2 IMPDHs using tiazofurin and ADP, which bind
110                                              Human type 2 innate lymphoid cells (ILC2s) are identifie
111                          Although a putative human type 2 iodothyronine deiodinase (D2) gene (hDio2)
112 anges in gene expression similar to those in human type 2 islets.
113                                 Samples from human type 2 NHBD and BDD were obtained at the end of co
114 acid protein that most closely resembles the human Type 2 phosphatidic acid phosphatase PAP-2c.
115                               Studies of the human type 2 receptor (AGTR2) gene in two independent co
116 in little change in the binding affinity for human type 2 receptor.
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
119                                           In humans, type 2 diabetes generally occurs when insulin-se
120                                              Human type 3 3alpha-hydroxysteroid dehydrogenase, or ald
121   Here, we report structural findings of the human type-3 IP(3)R (IP(3)R-3) obtained by cryo-EM (at a
122                         Purified recombinant human type 4 phosphodiesterase B2B (HSPDE4B2B) exists in
123 s were infected with a replication-deficient human type 5 adenovirus containing cDNA for SOD2.
124                                A recombinant human type 5 adenovirus containing the murine MIP-1alpha
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
132 site residues in the reaction catalyzed by a human-type ACA.
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.
135                           The mouse model of human type B Tay-Sachs disease recently engineered by th
136  an alternative catabolic pathway for GM2 in human type B Tay-Sachs patients.
137               Aged canines (dogs) accumulate human-type beta-amyloid (Abeta) in diffuse plaques in th
138                     We show that over 90% of human types correspond transcriptomically to those previ
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
141 trate specificity was similar to that of the human Type I 5PTase.
142 o, presumably by MIP-133 degradation of both human type I and human type IV collagen.
143 ve tumors that correlates with expression of human type I and III IFNs derived from the cancer cells.
144  Zucker diabetic fatty (ZDF) rats, models of human type I and type II diabetes, respectively.
145                              Ofatumumab is a human type I anti-CD20 antibody approved by the US Food
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
151 ed in several recombinant proteins including human Type I collagen polypeptides.
152                           When a six-triplet human type I collagen sequence containing GFPGER was int
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
157 onstitutes the first reported structure of a human type I IFN bound to a therapeutic antibody.
158   Interestingly, the interaction between the human type I IFN receptor and STAT1 is not direct but me
159                The cytoplasmic domain of the human type I IFN receptor chain 2 (IFNAR2c or IFN-alphaR
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
162                The crystal structures of two human type I IFN ternary signaling complexes containing
163                                      Sixteen human type I IFN variants signal through the same cell-s
164  for STAT4 recruitment and activation by the human type I IFNAR (IFN-alphabetaR), it is not sufficien
165                                          The human type I IFNs include one IFN-beta and multiple IFN-
166 e I interferons (IFNs), bovine IFNAR-1 binds human Type I IFNs with moderate (nM) affinity, and can b
167 required for the antiproliferative effect of human type I IFNs.
168 ey was capable of binding and activating the human type I IL-1 receptor.
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
172                We have mapped 36 SARs in the human type I interferon (IFN) gene complex on chromosome
173   Dromedary viruses were as sensitive to the human type I interferon response as HCoV-229E.
174  novel set of inborn errors of immunity, the human type I interferonopathies.
175 an IFNAR-1 has a weak intrinsic affinity for human Type I interferons (IFNs), bovine IFNAR-1 binds hu
176                                          The human type I interferons, IFN-alpha, IFN-beta, and IFN-o
177  to the existence of the mouse equivalent of human type I keratin 16 (K16).
178 e cotranslational maturation pathway for the human type I membrane glycoprotein tyrosinase.
179 were engineered with a constitutively active human type I Nodal receptor (caACVR1b) to mimic activati
180                             Depletion of the human type I phosphatidylinositol 4-phosphate 5-kinase b
181             In this study, the mechanisms of human type I PKG-alpha (PKG-Ialpha) gene expression were
182                                      A novel human Type I procollagen C-proteinase enhancer protein-l
183 oduce both propeptide chains that constitute human type I procollagen.
184 in, which associates with both SmRK1 and the human type I TGF beta receptor (T beta RI); overexpressi
185 K1 joined to the intracellular domain of the human type I TGF-beta receptor was used.
186                 The alpha(2)-I protein bound human types I and III collagen in a saturable and divale
187 sing simulated data for three model species: humans (type I survival), sparrow (type II), and barnacl
188                              We show that in humans, type I interferons induce TH1 development and ca
189 nd greatest on NIH 3T3 cells over-expressing human type-I IGF receptor.
190 PH); and 2) the ligand-binding domain of the human type-I IP3R (IP3R224-605).
191                             Mutations of the human type Ialpha regulatory subunit (RIalpha) of cyclic
192 ructural and mechanistic properties with the human type IB enzyme (hTopo) and is important for viral
193 ly available structures for the vaccinia and human type IB enzymes.
194       Previously we showed that infection of human type II airway epithelial (A549) cells with purifi
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
197 n extended to deficiency of adherence to the human type II alveolar cells.
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
200 nucleotide (I) is a potent inhibitor of both human type II and Escherichia coli IMPDH.
201  competitive inhibition of the mitochondrial human type II arginase by N(omega)-hydroxy-L-arginine, t
202        We also demonstrate the inhibition of human type II arginase by the boronic acid-based transit
203 BEC are classical, competitive inhibitors of human type II arginase with K(i) values of 0.25 and 0.31
204 as with prominent nuclear atypia, resembling human Type II cancers.
205 terleukin (IL)-8 from monolayers of cultured human type II cells was assessed.
206 with cartilage proteoglycan aggrecan (PG) or human type II collagen (CII) emulsified with Freund's co
207 tions of human cartilage gp-39 (HC gp-39) or human type II collagen (CII).
208 mmune arthritis induced by immunization with human type II collagen (hCII).
209 the immune response to collagen, recombinant human type II collagen (rCII) was produced using a yeast
210 mplexed with a candidate RA autoantigen, the human type II collagen peptide CII (259-273).
211 QB3 (H2A(q)) mice susceptible to porcine and human type II collagen-induced arthritis.
212 rotein was identified by Western blot with a human type II collagen-specific antibody.
213 ice when they are immunized with porcine and human type II collagen.
214 ith the primary collagenase cleavage site of human type II collagen.
215 h individual synthetic peptides representing human type II collagen.
216                      EPCs were isolated from human type II diabetics (n=20) and age-matched control s
217 orated random abasic sites into plasmid DNA, human type II enzymes can locate lesions even within a b
218 and stimulated DNA scission mediated by both human type II enzymes.
219 od vessels and mutations of the ALK1 gene in human type II hereditary hemorrhagic telangiectasia pati
220                                              Human type II hydroxyacyl-CoA dehydrogenase/amyloid-beta
221  human IL-1alpha and IL-1beta to the soluble human type II IL-1 receptor by approximately 100-fold, w
222 ormation of NADH bound to the active site of human type II IMPDH (IMPDH-h2).
223 up-regulated in rapidly proliferating cells, human type II IMPDH is actively targeted for immunosuppr
224  2.9-A structure of a ternary complex of the human type II isoform of IMPDH.
225 ntribute to the observed selectivity for the human Type II isoform.
226 for brain development and is associated with human type II lissencephaly.
227 ial cells and of both IAV and IBV in primary human type II pneumocytes.
228 tably transfected NIH 3T3 cells expressing a human type II procollagen gene under the control of the
229 e functional analysis of all six recombinant human type II skeletal muscle myosin isoforms.
230 ave selectively expressed a kinase-deficient human type II TGFbeta receptor (TbetaRIIDeltak) in fibro
231 had relatively low potency for inhibition of human type II topoisomerases alpha and beta.
232             Inhibition of one or both of the human type II topoisomerases by antibacterial compounds
233  model for the use of divalent metal ions by human type II topoisomerases.
234 he cellular and pharmacological functions of human type II topoisomerases.
235                              Exposure of the human-type II cell alveolar epithelial cells (A549) to D
236               The catalytic mechanism of the human type-II IMPDH isozyme has been studied by measurem
237 soforms in SCLC lines, as compared to normal human type-II pneumocytes.
238 spect, we have stably overexpressed FRA-1 in human type-II-like alveolar malignant cell line (A549) a
239                     The crystal structure of human type III 3alpha-hydroxysteroid dehydrogenase (HSD)
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
247                                         Anti-human type IV collagen basement membrane immunoreactivit
248            On the basis of our findings that human type IV collagen binds BMP4, we predict that this
249                           The NC1 domains of human type IV collagen, in particular alpha3NC1, are inh
250 MIP-133 degradation of both human type I and human type IV collagen.
251 milar to the consensus sequence are found in human type IV collagen.
252 present during the late elicitation phase of human type IV hypersensitivity reactions.
253                    In this study, we mutated human-type LT and STa genes, which are highly homologous
254                 This study demonstrated that human-type LT(1)(9)(2)-STa(1)(3) fusions induce neutrali
255 r oligosaccharides into structurally uniform human-type N-glycans.
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
258             The rNV VLPs hemagglutinated all human type O (11 of 11), A (9 of 9), and AB (4 of 4) RBC
259 ti-H type 2 antibody inhibited rNV VLP HA of human type O RBCs.
260 igen functions as the rNV VLP HA receptor on human type O RBCs.
261  these antigens also inhibited rNV VLP HA of human type O RBCs.
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
265 uent seasonal IAVs, and potential for future human-type receptor adaptation in novel avian HAs.
266 mics in humans, maintenance and evolution of human-type receptor specificity in subsequent seasonal I
267                 It is notable that acquiring human-type receptor specificity needs multiple amino aci
268                            The HA-sfGFP with human-type receptor specificity was able to bind to a gl
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
272                 HAs from human IAVs exhibit "human-type" receptor specificity, binding exclusively to
273 receptor-binding domain conferred binding to human-type receptors but reduced HA stability.
274                            Remarkably, these human-type receptors with elongated branches have the po
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,
278                       The ability to bind to human-type receptors, together with physical stability a
279 s possessing HA-222D preferentially bound to human-type receptors, while those encoding HA-222G bound
280 ses no longer have strict specificity toward human-type receptors.
281  and thus require adaptive mutations to bind human-type receptors.
282 se encoding HA-222G bound to both avian- and human-type receptors.
283  binding site, which is critical for binding human type sialic acid receptors.
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
286                              Probing for the human-type telomere (TTAGGG)n also revealed no signal.
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
289 cts with the N-terminal segments of hACV and human type VI adenylyl cyclase (hACVI).
290  displayed dipeptidase activity and degraded human type VI collagen and fibrinogen, but not salivary
291 se skin resulted in the stable expression of human type VII collagen at the mouse DEJ.
292                                          The human type VII collagen gene (COL7A1) recently has been
293 bullous disorders caused by mutations in the human type VII collagen gene (COL7A1).
294 y suggest that autoantibodies that recognize human type VII collagen in EBA are pathogenic.
295       In this study, we produced recombinant human type VII collagen in stably transfected human 293
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
299 N6 viruses have acquired a high affinity for human-type virus receptor.
300 tal structure of the trimerization domain of human type XVIII collagen, a member of the multiplexin f

 
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