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1 uring repeated, failed episodes of emergency granulopoiesis.
2 ibutes to genomic stability during emergency granulopoiesis.
3 matopoietic activity shifts toward promoting granulopoiesis.
4 n unexpected subtype-specific role for H1 in granulopoiesis.
5  novel important target of C/EBPalpha during granulopoiesis.
6 L-1beta, an essential cytokine for emergency granulopoiesis.
7 he development of neutrophil immunity during granulopoiesis.
8 progenitors and that exogenous RUNX1 rescues granulopoiesis.
9 structive lesions of the spleen and impaired granulopoiesis.
10 d promoter histone acetylation, and inhibits granulopoiesis.
11 rvival but have little impact on bone marrow granulopoiesis.
12 ion with G193X Elane, had no effect on basal granulopoiesis.
13  plays a key role in stimulating bone marrow granulopoiesis.
14 es production of cytokines that drive excess granulopoiesis.
15 control to G-CSF signaling and regulation of granulopoiesis.
16 i1 and G-CSF are linked in the regulation of granulopoiesis.
17 of C/EBPalpha occupancy during demand-driven granulopoiesis.
18 rentiation and the homeostatic regulation of granulopoiesis.
19 yeloid progenitor compartments to accelerate granulopoiesis.
20 ccelerated granulopoiesis known as emergency granulopoiesis.
21 role for their proliferation in inflammatory granulopoiesis.
22 tor cells but did not rescue Gfi1-/- blocked granulopoiesis.
23 lymphocytes from the BM along with increased granulopoiesis.
24 ion of myeloid progenitors, but not terminal granulopoiesis.
25 SCN patient) completely blocks G-CSF-induced granulopoiesis.
26 colony-stimulating factor (G-CSF)-stimulated granulopoiesis.
27 le receptor (sIL6R) contributes to emergency granulopoiesis.
28 ulted in a dominant-negative block to murine granulopoiesis.
29  acid receptor (RAR) and C/EBPepsilon direct granulopoiesis.
30  differentiation, including myelopoiesis and granulopoiesis.
31  little is known about the role of miRNAs in granulopoiesis.
32 penia (CN), a related but milder disorder of granulopoiesis.
33  dominant, cell-intrinsic fashion to disrupt granulopoiesis.
34 of cyclic neutropenia, a related disorder of granulopoiesis.
35 l neutropenia (SCN) is an inborn disorder of granulopoiesis.
36 genital neutropenia is an inborn disorder of granulopoiesis.
37     In vivo expression profoundly stimulates granulopoiesis.
38 hematopoietic stem cells in a process called granulopoiesis.
39 , and 67% of ET patients demonstrated clonal granulopoiesis.
40 anscriptional repressor that is required for granulopoiesis.
41 se signals regulate basal and stress-induced granulopoiesis.
42 d immunity involving appropriate rewiring of granulopoiesis.
43 yeloid disorders characterized by a block in granulopoiesis.
44 (G-CSF) is the principal cytokine regulating granulopoiesis.
45 ic differentiation, but downregulated during granulopoiesis.
46  favors monocyte differentiation by blocking granulopoiesis.
47 SF), consistent with their critical roles in granulopoiesis.
48 he C/EBPalpha basic region, are required for granulopoiesis.
49 o granulocytes in steady-state and emergency granulopoiesis.
50 ancer binding protein alpha) is critical for granulopoiesis.
51 forming unit and mature neutrophil stages of granulopoiesis.
52 dicative of "glycosylation by timing" during granulopoiesis.
53 onent of G-CSF-driven cell proliferation and granulopoiesis.
54 g induction of other C/EBP family members in granulopoiesis.
55 of chemotherapy patients through accelerated granulopoiesis.
56 dentifying zebrafish mutants with defects in granulopoiesis.
57 CSF) plays a major role in the regulation of granulopoiesis.
58 e form of stem cell factor (SCF) for optimal granulopoiesis.
59 MPO maturation occurs during early/mid-stage granulopoiesis.
60 rmation of monocyte/macrophages and enhanced granulopoiesis.
61  phenotype, with dramatic effects on in vivo granulopoiesis.
62 d event in patients with pre-existing clonal granulopoiesis.
63 clearance, neutrophil release, and emergency granulopoiesis.
64  targeting immunosuppressive neutrophils and granulopoiesis.
65 olymicrobial sepsis, by supporting emergency granulopoiesis.
66 ular emphasis on the role of neutrophils and granulopoiesis.
67  Egr-2 may contribute to the role of Gfi1 in granulopoiesis.
68 ioenergetic changes which underpin emergency granulopoiesis.
69  progenitor cell surface glycans to suppress granulopoiesis.
70  ZBTB11, as critical for basal and emergency granulopoiesis.
71  understand the glycosylation process during granulopoiesis.
72 tially expressed >2-fold throughout terminal granulopoiesis.
73  for G-CSF as the main mediator of emergency granulopoiesis.
74 bp/Irf8) was required to terminate emergency granulopoiesis.
75 cols that recapitulate the major features of granulopoiesis.
76 epithelium in the outer medulla can regulate granulopoiesis.
77 capitulated the patient's clinical arrest in granulopoiesis.
78 uced Triad1 expression on emergency (stress) granulopoiesis.
79 sponse nor significantly alters steady-state granulopoiesis.
80 yeloid progenitor expansion during emergency granulopoiesis.
81  iPSCs through C/EBPbeta-dependent emergency granulopoiesis.
82 f G-CSF receptor-mediated signaling in human granulopoiesis.
83 the timed expression of C/EBP-epsilon during granulopoiesis.
84 iferation, cell cycle, and maturation during granulopoiesis.
85  generally show decreased methylation during granulopoiesis.
86 on of systemic infection into demand-adapted granulopoiesis.
87 ds of wild-type (WT) mice exhibited impaired granulopoiesis.
88 s,thereby directly linking TLR-triggering to granulopoiesis.
89 so found that repeated episodes of emergency granulopoiesis accelerated progression to acute myeloid
90                             Basal and stress granulopoiesis after myeloablative therapy are normal in
91 e mechanism that is required for recovery of granulopoiesis after radiation injury.
92 -1+/c-kit+ cells produced PGE2 and underwent granulopoiesis after TLR2 stimulation.
93                                    Emergency granulopoiesis also hastened postchemotherapy relapse in
94 ting protein glycosylation during neutrophil granulopoiesis and a more detailed understanding of neut
95                   IL-17A and IL-17F regulate granulopoiesis and are produced by memory T cells.
96 s signal to the BM via resolvins to regulate granulopoiesis and BM neutrophil deployment.
97  AT, and translated into reduced bone marrow granulopoiesis and cardiac neutrophil infiltration 3 day
98 e of inhibition of proliferative pathways in granulopoiesis and demonstrate that several regions of t
99 lude that AT-induced IL-1beta promotes local granulopoiesis and effective resolution of S. aureus-inf
100 scription factor C/EBP alpha is required for granulopoiesis and frequently disrupted in human acute m
101 -21 has been implicated in the regulation of granulopoiesis and hepatic gene expression.
102 ings demonstrate an essential role for AR in granulopoiesis and host defense against microbial infect
103  coinhibitory receptor for G-CSFR regulating granulopoiesis and host innate immune response to bacter
104 nto Ceacam1(-/-) bone marrow restored normal granulopoiesis and host sensitivity to LM infection, whi
105 al network controlled by C/EBPepsilon during granulopoiesis and identifies Trem1 as one of its downst
106 stream signaling cascade suppress MI-induced granulopoiesis and improve cardiac function.
107  target pathways in neutrophils required for granulopoiesis and innate immunity.
108  alpha (C/EBPalpha) is a master regulator in granulopoiesis and is frequently disrupted in acute myel
109 ligase required for termination of emergency granulopoiesis and leukemia suppressor function in MLL1-
110 on of Bcl3 in recipients inhibited emergency granulopoiesis and limited acute graft damage.
111                          We demonstrate that granulopoiesis and lymphopoiesis are coupled specificall
112 w that STAT3 has a crucial role in emergency granulopoiesis and mature neutrophil function.
113 c finger transcription factor that regulates granulopoiesis and may have a regulatory role in cellula
114 , interleukin-1beta) in neutrophils suppress granulopoiesis and may improve cardiac function in patie
115 that restricted erythropoiesis but permitted granulopoiesis and megakaryopoiesis.
116 cific cytokines that play a dominant role in granulopoiesis and monopoiesis, respectively.
117 chemic graft storage enhances G-CSF-mediated granulopoiesis and neutrophil graft infiltration, result
118 ection and neutrophil homeostasis, including granulopoiesis and neutrophil release from the bone marr
119 th transcriptomic and epigenetic rewiring of granulopoiesis and neutrophil reprogramming toward an an
120  important regulator of host defense through granulopoiesis and neutrophil trafficking.
121 neutrophil apoptosis, the role of CEACAM1 in granulopoiesis and neutrophil-dependent host immune resp
122        Integrin alpha9beta1 was required for granulopoiesis and played a permissive role in the G-CSF
123 hich fail to develop lobulated nuclei during granulopoiesis and present an in vitro model for Pelger-
124 e gain-of-function of Stat5 causes excessive granulopoiesis and prolonged survival of granulocytes in
125 sh Lyn and Hck as key negative regulators of granulopoiesis and raise the possibility that loss of Sr
126 rovide direct evidence for STAT3-independent granulopoiesis and suggest that STAT3 directs a negative
127 itical role for Bcl3 in regulating emergency granulopoiesis and suggest that targeting the differenti
128 nd transcriptional changes that occur during granulopoiesis and supports the role of DNA methylation
129 prominent role of IL-23 in the regulation of granulopoiesis and the prevalence of IL-17A-producing Tn
130 em, can result in a differentiation block in granulopoiesis and thus contribute to leukemic transform
131 role specifically for the SMARCD2 subunit in granulopoiesis, and further investigation implicates the
132      They also displayed enhanced entry into granulopoiesis, and inhibited postmitotic terminal diffe
133 ances 32D cell survival, promotes entry into granulopoiesis, and inhibits postmitotic differentiation
134 y CXCL1 as a central player in host defense, granulopoiesis, and mobilization of neutrophils during G
135 s role in regulating neutrophil recruitment, granulopoiesis, and neutrophil mobilization in response
136 vestigate the role of CXCL1 in host defense, granulopoiesis, and neutrophil mobilization.
137 sis, delayed leukemogenesis during emergency granulopoiesis, and normalized innate immune responses w
138 rdial AT coordinates immune cell activation, granulopoiesis, and outcome after MI.
139  vivo G-CSF levels and stimulation of marrow granulopoiesis, and was comparable to that of exogenousl
140                   Steady-state and emergency granulopoiesis are both dependent on TLR signaling.
141 ular events involved in initiating emergency granulopoiesis are known, but termination of this proces
142 isms controlling infection-induced emergency granulopoiesis are poorly defined.
143  mechanisms by which these mutations disrupt granulopoiesis are unclear.
144 rowth factor that has a role in steady state granulopoiesis, as well as in mature neutrophil activati
145 y be clinically useful to enhance neutrophil granulopoiesis, as well as to study the mechanisms invol
146 ed reduction of Stat3 amounts rescued normal granulopoiesis, attenuating host sensitivity to LM infec
147  normal progenitors, C/EBPs are required for granulopoiesis beyond their ability to induce receptors
148 , B cells vacate the marrow during emergency granulopoiesis but return upon restoration of homeostasi
149 l elastase in providing negative feedback to granulopoiesis by direct antagonism of G-CSF.
150 roduction, but also the disruption to normal granulopoiesis by excessive ST6GAL1 in malignancy.
151  STAT3 as an essential mediator of emergency granulopoiesis by its regulation of transcription factor
152 rovide evidence that the G-CSFR may regulate granulopoiesis by several mechanisms.
153 a and miR-182 for the maintenance of healthy granulopoiesis.C/EBPalpha is a critical transcription fa
154 ed in hypoxic response (Hif1a) and emergency granulopoiesis (Cebpb).
155 h these mice did not display the increase in granulopoiesis commonly found in chronic myeloid leukemi
156 sis in the blood under both basal and stress granulopoiesis conditions primarily by regulating neutro
157                      The observed failure of granulopoiesis could be rescued by the addition of solub
158 f TRIAD1-substrate RTKs terminated emergency granulopoiesis, delayed leukemogenesis during emergency
159 nt mice have a severe quantitative defect in granulopoiesis despite which phenotypically normal neutr
160 tive of neutrophil homeostasis and emergency granulopoiesis determined by innate immunologic signalin
161 igation of the effect of C/EBPalphap30-ER on granulopoiesis downstream of G-CSF signalling, we coexpr
162 ere we showed that neutrophils and emergency granulopoiesis drove a maladaptive response during sepsi
163 plays a critical role in mediating emergency granulopoiesis during acute infection.
164                         Impaired bone marrow granulopoiesis during burn sepsis often results in neutr
165 mulating factor (G-CSF) mediates "emergency" granulopoiesis during infection, a process that is mimic
166                                    Emergency granulopoiesis during peritonitis evoked changes in BM r
167 1 activity, impairs termination of emergency granulopoiesis during the innate immune response and con
168 ions or adjuvant usage can trigger emergency granulopoiesis (EG), leading to dysregulation in neutrop
169 the interrelated processes of hematopoiesis, granulopoiesis, erythropoiesis, and lymphopoiesis.
170 he bone marrow via the circulation and local granulopoiesis from hematopoietic stem and progenitor ce
171 her blood cell lineages, its function during granulopoiesis has remained elusive.
172 t drive reactive neutrophilias and emergency granulopoiesis have been inferred but not demonstrated.
173 dition, some ET and MMM patients with clonal granulopoiesis have somatic mutations other than JAK2V61
174 ltiple hematopoietic cytokines can stimulate granulopoiesis; however, their relative importance in vi
175  neutrophil homeostasis in the steady state, granulopoiesis in 'emergency' conditions and interaction
176 ranulocyte colony-stimulating factor-induced granulopoiesis in 32D cells or retinoic acid- and vitami
177 beta-ER or C/EBPdelta-ER can induce terminal granulopoiesis in 32D cl3 cells.
178 itor cells in the bone marrow and stimulates granulopoiesis in a cell-autonomous manner.
179 his, we found aberrantly sustained emergency granulopoiesis in a murine model of MLL1-rearranged AML,
180                         IL-23 also regulates granulopoiesis in a neutrostat regulatory feedback loop
181  the accumulation of Bcl3 protein attenuated granulopoiesis in an NF-kappaB p50-dependent manner.
182 an and rodents and is essential for terminal granulopoiesis in both species.
183 ta in granulopoiesis; therefore, we examined granulopoiesis in C/EBPbeta-deficient mice.
184 ction of cells with COPZ2 restored defective granulopoiesis in COPZ1-mutated human CD34+ cells, offer
185                                      Altered granulopoiesis in DeltaNC16A mice is through bone marrow
186            Blockade of G-CSF restored normal granulopoiesis in DeltaNC16A mice.
187                             Failed emergency granulopoiesis in Fancc(-/-) mice was associated with ex
188       Blocking neutrophilia during emergency granulopoiesis in Fancc(-/-)Tp53(+/-) mice (but not WT)
189 cently been shown to have a critical role in granulopoiesis in humans, mice, and zebrafish.
190 r neutrophils during G-CSF-induced emergency granulopoiesis in humans.
191 on of G-CSF in vivo, as a model of emergency granulopoiesis in humans.
192 emonstrated that the early increase in human granulopoiesis in NSG-3GS mice reflects an expanded outp
193 ggesting that TLR2/MyD88 activation promotes granulopoiesis in part by production and autocrine activ
194 d for induction of C/EBPalpha expression and granulopoiesis in response to G-CSF or other cytokines i
195                             We conclude that granulopoiesis in S aureus-infected wounds is induced by
196 nsight into the mechanism underlying reduced granulopoiesis in the absence of NF-kappaB p50, we asses
197 enrichment is likely reflective of increased granulopoiesis in the bone marrow and not peripheral neu
198  (-/-) mice demonstrated impaired neutrophil granulopoiesis in the bone marrow intrinsically and afte
199                                       During granulopoiesis in the bone marrow, distinct neutrophil g
200 rculation and in the liver, through enhanced granulopoiesis in the bone marrow.
201 ut they initiate differentiation and undergo granulopoiesis in the presence of granulocyte CSF (G-CSF
202 ogenitors showed decreased emergency-induced granulopoiesis in vitro and in vivo.
203 reduces C/EBPalpha protein level and impairs granulopoiesis in vitro and in vivo.
204 3, elastase, azurocidin, and cathepsin G) on granulopoiesis in vitro.
205  role for the G-CSFR as a major regulator of granulopoiesis in vivo and provide evidence that the G-C
206 ate that IL-6 is an independent regulator of granulopoiesis in vivo and show that neither G-CSFR or I
207 nt mice; moreover, exogenous IL-6 stimulated granulopoiesis in vivo in the absence of G-CSFR signals.
208  role for the G-CSFR as a major regulator of granulopoiesis in vivo, but also indicated that G-CSFR i
209 urine IL-17 is a cytokine that can stimulate granulopoiesis in vivo.
210    This pattern is consistent with "reactive granulopoiesis," in which committed myeloid progenitors
211  slowed G1, but did not induce early or late granulopoiesis, indicating that cell cycle inhibition as
212                           In vitro models of granulopoiesis involving the inducible expression of eit
213                                    Emergency granulopoiesis is a component of the innate immune respo
214                               'Steady-state' granulopoiesis is absolutely dependent on the C/EBPalpha
215 oid progenitors accumulate, whereas terminal granulopoiesis is blocked.
216  we demonstrate that this specialization for granulopoiesis is determined by inflammation-induced red
217  mouse lung allografts unless G-CSF-mediated granulopoiesis is inhibited.
218  myeloid maturation, indicating that resting granulopoiesis is normal.
219 ates that conversion to a state of emergency granulopoiesis is temporally delayed, allowing B cells o
220                                              Granulopoiesis is under the control of transcriptional f
221 to the switch from steady-state to emergency granulopoiesis is, however, unknown.
222 timulating factor (G-CSF) receptor-triggered granulopoiesis, is downregulated in granulocytic progeni
223  that NFI-A promoter silencing, which allows granulopoiesis, is guaranteed by epigenetic events, incl
224 ed by a hematopoietic program of accelerated granulopoiesis known as emergency granulopoiesis.
225 etics of infection, circulating blood cells, granulopoiesis, lesions, and cellular populations in the
226                        Our findings identify granulopoiesis-mediated augmentation of alloimmunity as
227                     Rather than a deficit in granulopoiesis, mice lacking STAT3 in their hematopoieti
228 pment (miR-150 and miR-17 approximately 92), granulopoiesis (miR-223), immune function (miR-155) and
229                                       During granulopoiesis, miR-223 localizes inside the nucleus and
230 L; p<0.0001), bone marrow erythropoiesis and granulopoiesis, more venous thromboses, and a higher rat
231 C/EBPalpha(BRM2)-ER induced early markers of granulopoiesis much less efficiently than C/EBPalpha-ER
232 icated that G-CSFR independent mechanisms of granulopoiesis must exist.
233 uggest that G-CSFR-independent mechanisms of granulopoiesis must exist.
234 le for Runx1 tyrosine phosphorylation during granulopoiesis, mutation of the five Src-modified residu
235                                    Emergency granulopoiesis occurs in response to infectious or infla
236                       Here, through directed granulopoiesis of gene-edited isogenic normal and patien
237 colony-stimulating factor (G-CSF) to promote granulopoiesis of human hematopoietic stem cells (HSCs),
238 regulation of C/EBPalpha by microRNAs during granulopoiesis or acute myeloid leukemia development has
239 he disruption of CD18 functions essential to granulopoiesis or basal leukocyte trafficking.
240 ers normal leukocyte production by promoting granulopoiesis over lymphopoiesis, a response that suppo
241 nt by evicting resident B cells and favoring granulopoiesis over lymphopoiesis.
242 hopoiesis, and higher C/EBP levels may favor granulopoiesis over monopoiesis.
243 row into TTP KO mice and found the "reactive granulopoiesis" phenocopied, indicating a non-hematopoie
244 ling compromised activation of the emergency granulopoiesis program, which requires maintenance and e
245   Moreover, we also identified C/EBPalpha, a granulopoiesis-promoting transcription factor, as a subs
246                                    Emergency granulopoiesis refers to the increased production of neu
247 ne expression pattern with overexpression of granulopoiesis-related and interferon (IFN)-induced gene
248 nscriptional mechanisms underlying emergency granulopoiesis remain unclear.
249  stage, whereas progenitor cell expansion or granulopoiesis remained unimpaired.
250 -/-) non-granulated defect and suggests that granulopoiesis requires a structural motif that is conse
251   In this study, we show that IL-17-mediated granulopoiesis requires G-CSF release and the presence o
252                                        Early granulopoiesis requires the C/EBPalpha, PU.1, RAR, CBF,
253 uction or silencing boosts erythropoiesis or granulopoiesis, respectively.
254 xhibited an overwhelming and fatal emergency granulopoiesis response that was characterized by tissue
255 echanisms of STAT3 function in the emergency granulopoiesis response to G-CSF administration or infec
256                                   The stress granulopoiesis response, as measured by neutrophil recov
257 /EBPbeta), a crucial factor in the emergency granulopoiesis response.
258 (-/-) mice after stimulation of an emergency granulopoiesis response.
259 G-CSF-independent effect of IL-17 on splenic granulopoiesis, resulting in a preservation of mature ci
260  accumulation was attributable to attenuated granulopoiesis secondary to assessed lower levels of IL-
261 unaffected in CN, suggests the presence of a granulopoiesis-specific mechanism downstream of G-CSF re
262                                          The granulopoiesis-stimulating agents (GSAs) have been effec
263 bed role for HoxA10 in terminating emergency granulopoiesis, suggesting an important contribution by
264 iant unable to bind NF-kappaB p50 stimulated granulopoiesis, suggesting their cooperation with C/EBPa
265 nt analysis, including greater expression of granulopoiesis, T-cell and IFN signaling, and integrated
266 in myeloid cells, are negative regulators of granulopoiesis that act at distinct stages of granulocyt
267 l neutropenia (SCN) is an inborn disorder of granulopoiesis that in many cases is caused by mutations
268 topoietic response program termed "emergency granulopoiesis" that is characterized by increased de no
269 than the hours required to induce "emergency granulopoiesis," the relevance of having high numbers of
270 ttle is known about the role of C/EBPbeta in granulopoiesis; therefore, we examined granulopoiesis in
271 n to the effect of THP on the epithelium and granulopoiesis, this new immunomodulatory role could exp
272 e show that IL-17, a cytokine that regulates granulopoiesis through G-CSF, is made by gammadelta T ce
273                    IL-23 and IL-17A regulate granulopoiesis through G-CSF, the main granulopoietic cy
274 idence that BP180 plays an important role in granulopoiesis through regulating NF-kappaB signaling pa
275  proteins act as dominant negatives to block granulopoiesis through selective deregulation of a subse
276                          Cytokines stimulate granulopoiesis through signaling via receptors whose exp
277 ibit the alternate cell fate choice, that of granulopoiesis, through inhibition of C/EBPalpha.
278 marrow, which comprise a myeloid bias toward granulopoiesis together with decreased B-lymphopoiesis.
279 tor B cell leukemia/lymphoma 3 (Bcl3) limits granulopoiesis under emergency (i.e., inflammatory) cond
280 the transcriptional mechanisms that regulate granulopoiesis under inflammatory conditions are poorly
281 ed that nMPO is dynamically expressed during granulopoiesis, unevenly distributed across granules and
282 n DNA methylation and gene expression during granulopoiesis using 4 distinct cell populations ranging
283 have assessed the effect of C/EBPalphap30 on granulopoiesis utilizing C/EBPalphap30-ER, containing th
284 nd SHP2, potentially shifting the balance to granulopoiesis via gene induction by C/EBPalpha homodime
285 principally by CD4(+) T cells, which induces granulopoiesis via granulocyte colony-stimulating factor
286 -tumor effect of beta-glucan-induced trained granulopoiesis was transmissible by bone marrow transpla
287               After stimulation of emergency granulopoiesis, we found increased and sustained express
288  explore the role of interleukin-6 (IL-6) in granulopoiesis, we generated IL-6 x G-CSFR doubly defici
289 h lamin A is typically down-regulated during granulopoiesis, we genetically modified HL-60 cells to g
290 To delineate the role of C/EBPalpha in human granulopoiesis, we studied its expression and function i
291 igate the effects of mutant NE expression on granulopoiesis, we used the HL-60 promyelocytic cell lin
292 B (interleukin-1B), the effector molecule in granulopoiesis, were not affected by MI, suggesting that
293 interleukin-1beta), the effector molecule in granulopoiesis, were not affected by MI, suggesting that
294 omatic repression of NFI-A gene and channels granulopoiesis, whereas its stable knockdown produces th
295  aureus-infected skin wounds in mice undergo granulopoiesis, whereas other authors have demonstrated
296 ve Stat5 in diseased animals restored normal granulopoiesis, which also resulted in a swift clearance
297 critical function for C/EBPbeta in emergency granulopoiesis, which demands both differentiation and p
298       Although C/EBPalpha is known to induce granulopoiesis while suppressing monocyte differentiatio
299 fut1(-/-) embryonic stem cells show enhanced granulopoiesis with depressed lymphoid lineage developme
300 xamined this pathway in HSPC trafficking and granulopoiesis within S aureus-infected wounds.

 
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