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1 nding partner peptidyl-arginine deiminase 4 (PADI4).
2 NETs) through peptidyl arginine deiminase 4 (PADI4).
3 ated with the RA susceptibility haplotype of PADI4.
4  and bone-marrow-specific arginine deiminase PADI4.
5 es a toolkit for the study and modulation of PADI4 across (patho)physiological contexts.
6      Despite detailed molecular knowledge of PADI4 activation in vitro, we lack understanding of its
7 reflect the mechanism that promotes cellular PADI4 activation.
8  cellular PADI4; and PADI4_11, a cell-active PADI4 activator.
9 essor 4E-BP1 and reveal a cross-talk between PADI4 activity and 4E-BP1 phosphorylation.
10                                              PADI4 activity limited the number of cancer stem cells (
11 tiated hair lineage cells and indicates that PADI4 acts to repress transcription during hair follicle
12                                              PADI4 additionally mediates immune responses and cellula
13                                              PADI4 (also called PAD4 or PADV), the only PADI with a n
14 cle development to delineate the function of PADI4, an enzyme converting peptidylarginine to citrulli
15 appaB inhibition depletes hRpn13 interactors PADI4 and HDAC8.
16 duces histone citrullination at HREs that is PADI4 and HIF dependent.
17           We further demonstrate how eQTL in PADI4 and NOD2 delineate risk variant function in rheuma
18 lise for the isolation and study of cellular PADI4; and PADI4_11, a cell-active PADI4 activator.
19 hat the expression and enzymatic activity of Padi4 are also induced under conditions of ground-state
20                                 We establish PADI4 as a negative regulator of proliferation, acting o
21         Our findings reveal a novel role for PADI4 as a tumor suppressor in regulating breast cancer
22 sults provide support for PTPN22, CTLA4, and PADI4 as RA susceptibility genes and demonstrate novel a
23                                              PADI4 binds and citrullinates hRpn13 and proteasomes, an
24  and illustrate how chromatin modifiers like PADI4 can direct the p53 transcriptional response.
25                Peptidylarginine deiminase 4 (PADI4) catalyzes the deimination of histone arginine res
26 d previously reported non-HLA signals around PADI4, CD28 and LIMK1.
27                                 We show that PADI4 citrullinates p53 at the C terminus in vitro, and
28 n this issue, Indeglia et al.(1) reveal that PADI4 citrullinates p53, redirecting its binding to ETS
29                             Mechanistically, PADI4 citrullinates proteins associated with mRNA proces
30 translational effectors, we demonstrate that PADI4 citrullinates the translational repressor 4E-BP1 a
31           Peptidylarginine deiminase 4 (PAD4/PADI4) counteracts the functions of protein Arg methyltr
32 for intraductal aggregate formation and that PADI4-deficiency abrogates disease progression.
33                                              Padi4 deletion did not prevent diet-induced dysbiosis, b
34  HIF target genes in breast cancer cells are PADI4 dependent.
35 cer cells in a peptidylarginine deiminase 4 (Padi4) dependent manner.
36                 Inhibition of neutrophils or Padi4-dependent NETosis phenocopies IL17 neutralization.
37   However, in sorted tumor cell populations, PADI4 downregulated expression of master transcription f
38                                              PADI4 enzymatically converts peptidyl-arginine to peptid
39 ipitation sequencing (ChIP-seq) reveals that PADI4 expression causes a redirection of p53 away from a
40                                              PADI4 expression is correlated with HIF-1a expression an
41                    Here, we demonstrate that PADI4 expression is induced by hypoxia in a HIF-dependen
42                           However, Padi2 and Padi4 expression was diminished in mature mTECs from NOD
43 1R [false discovery rate (FDR) = 5.4e-5] and PADI4 [FDR = 5.4e-5]) and neutrophil abundance (FDR = 9.
44 4_92*G/C, and padi4_104*T/C), mapping to the PADI4 gene and defining a haplotype previously reported
45                         Polymorphisms in the PADI4 gene influence the immune response to the PAD-4 pr
46 ingle-nucleotide polymorphisms (SNPs) in the PADI4 gene with RA in a UK population.
47 stocompatibility complex region and from the PADI4 gene.
48 pe of the peptidylarginine deiminase 4 gene (PADI4) has recently been identified as a gene conferring
49 oreover, a PROTAC against hRpn13 co-depletes PADI4, histone deacetylase HDAC8, and DNA methyltransfer
50 driver analysis identifies six genes (LTB4R, PADI4, IL1R2, PPP1R3D, KLHL2, and ECHDC3) predicted to c
51                Single-cell sequencing places Padi4 in both progenitor and differentiated hair lineage
52 ide insight into context-specific effects of PADI4 in epigenetic modulation.
53 consistent with a tumor-suppressive role for PADI4 in estrogen receptor-positive tumors.
54                                     Deleting Padi4 in hematopoietic cells (Padi4KO) blunted liver and
55                Higher expression of IL17 and PADI4 in human PDAC corresponds with poorer prognosis, a
56 sis, thereby uncovering a druggable role for PADI4 in mediating the metabolic effects of unhealthy mi
57 ptidylarginine deiminase 4 (PAD4, encoded by Padi4 in mice), an enzyme important in chromatin deconde
58    Here, we investigated a possible role for PADI4 in regulating breast cancer stem cells.
59  novel activity of the citrullinating enzyme PADI4 in suppressing breast cancer stem cells through ep
60 ullination by peptidyl arginine deiminase-4 (PADI4) in contact to particulate agents to extrude decon
61                                              PADI4, in turn, is recruited by HIFs to hypoxia response
62 hRpn13 and proteasomes, and proteasomes from PADI4-inhibited myeloma cells exhibit reduced peptidase
63                       Finally, pharmacologic PADI4 inhibition recapitulated findings obtained in Padi
64                             Mechanistically, PADI4 inhibition resulted in a widespread redistribution
65 e signature reflecting tumor cell-autonomous PADI4 inhibition was associated with poor outcome in hum
66 ET, and this could be prevented by selective PADI4 inhibition, demonstrating that this test does not
67               Peptidyl arginine deiminase 4 (PADI4) inhibition in mice blocked NETosis and resulted i
68            Experimental models indicate that PADI4 is critical for intraductal aggregate formation an
69                                              Padi4 is part of the pluripotency transcriptional networ
70                                              PADI4 is required for breast and liver tumor growth and
71 ne deiminase family member PAD4 (also called PADI4) is markedly overexpressed in a majority of human
72                          We hypothesize that PADI4 mediates the interactions between diet-modified mi
73             Wound healing was accelerated in Padi4(-/-) mice as compared to WT mice, and it was not c
74                                              Padi4(-/-) mice exhibited attenuated hypertension, reduc
75                            NETosis-deficient Padi4(-/-) mice were treated with Ang II (angiotensin II
76 NETs in wounds, but this was not observed in Padi4(-/-) mice.
77 elop and apply a set of potent and selective PADI4 modulators.
78         Interestingly, epigenetic effects of PADI4 on the bulk tumor cell population did not explain
79 ntrast with known tumor-promoting effects of PADI4 on the tumor stroma and suggest that the balance b
80               Peptidylarginine deiminase IV (PADI4, PAD4) deregulation promotes the development of au
81 itor specific for the active conformation of PADI4; PADI4_7, an inert binder, which we functionalise
82  of CTLA4 (CT60 allele, OR 1.23; P=.001) and PADI4 (PADI4_94, OR 1.24; P=.001) with the development o
83  anti-ACE2, B2G1, C1q, IFNalpha1, IFNalpha2, PADI4, PF4 and PR3 autoantibodies in hospitalized patien
84 essing and ribosomal biogenesis, and lack of PADI4 promotes protein synthesis and ribosomal RNA trans
85 his work contributes to our understanding of PADI4 regulation and provides a toolkit for the study an
86 rotein modification; suggestively, Padi2 and Padi4 RNA expression was correlated with arthritis sever
87 eonatal peptidyl arginine deiminase type IV (Padi4)-specific thymocytes reveal disparate fate choices
88                                 In contrast, Padi4-specific T cell receptors with short dwell times a
89                                  Temporally, Padi4-specific thymocytes are subject to a developmental
90 he generation of compact chromatin, as novel PADI4 substrates.
91                                            A PADI4 susceptibility haplotype associated with RA in a J
92 nes include LTF, LCN2, MMP9, S100A8, S100A9, PADI4, TGFBI, and CYBB.
93 obank data revealed that genetic variants in PADI4 that associated with increased risk of rheumatoid
94           Thus, HIF-dependent recruitment of PADI4 to target genes and local histone citrullination a
95                Citrullination of histones by PADI4 was recently implicated in regulating embryonic st
96 xpressing T cell receptors that engage IA(b)-Padi4 with moderate dwell times within a conventional do