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Template:PBB Cluster of differentiation antigen 135 (CD135) also known as Fms-like tyrosine kinase 3 (FLT-3) or receptor-type tyrosine-protein kinase FLT3 is a protein that in humans is encoded by the FLT3 gene. FLT-3 is a cytokine receptor expressed on the surface of hematopoietic progenitor cells.

Synonyms

fms-like tyrosine kinase receptor-3 (Flt3), fetal liver kinase-2 (Flk2)

Cell surface marker

Cluster of differentiation (CD) molecules are markers on the cell surface, as recognized by specific sets of antibodies, used to identify the cell type, stage of differentiation and activity of a cell. CD135 is an important cell surface marker used to identify certain types of hematopoietic (blood) progenitors in the bone marrow. Specifically, multipotent progenitors (MPP) and common lymphoid progenitors (CLP) express high surface levels of CD135. This marker is therefore used to differentiate hematopoietic stem cells (HSC), which are CD135 negative, from MPPs, which are CD135 positive.

Ligand

CD135 is the receptor for the cytokine Flt3 ligand (Flt3L).

Function

CD135 is a receptor tyrosine kinase type III. When this receptor binds to Flt3L it forms a dimer with itself (homodimer) that activates its intrinsic tyrosine kinase activity, which in turn phosphorylates and activates signal transduction molecules that propagate the signal in the cell. Signaling through CD135 plays a role in cell survival, proliferation, and differentiation. CD135 is important for lymphocyte (B cell and T cell) development, but not for the development of other blood cells (myeloid development).

Role in cancer

CD135 is a proto-oncogene, meaning that mutations of this protein can lead to cancer^[1]. Mutations of the Flt3 receptor can lead to the development of leukemia, a cancer of bone marrow hematopoietic progenitors. Internal tandem duplications of Flt3 (Flt3-ITD) are the most common mutations associated with acute myelogenous leukemia (AML) and are a prognostic indicator associated with adverse disease outcome.

AC220 and midostaurin are in phase II clinical trials for AML patients with FLT3 mutations.^[2]^[3]

Sorafenib has been reported to show significant activity against Flt3-ITD positive acute myelogenous leukemia.^[4]^[5]

References

^ FLT3 (FMS-like tyrosine kinase 3)
^ http://clinicaltrials.gov/ct2/show/NCT00989261 "Efficacy Study for AC220 to Treat Acute Myeloid Leukemia (AML) (ACE)"
^ http://www.genengnews.com/news/bnitem.aspx?name=71385927 "Astellas Pays $40M Up Front to Develop Ambit’s FLT3 Kinase Inhibitors"
^ http://www.ncbi.nlm.nih.gov/pubmed/19389879
^ http://www.medscape.com/viewarticle/573902_4

External links

CD135+Antigen at the U.S. National Library of Medicine Medical Subject Headings (MeSH)

Template:PBB Controls

[1] FLT3 (FMS-like tyrosine kinase 3)

[2] ttp://clinicaltrials.gov/ct2/show/NCT00989261 "Efficacy Study for AC220 to Treat Acute Myeloid Leukemia (AML) (ACE)"

[3] ttp://www.genengnews.com/news/bnitem.aspx?name=71385927 "Astellas Pays $40M Up Front to Develop Ambit’s FLT3 Kinase Inhibitors"

[4] ttp://www.ncbi.nlm.nih.gov/pubmed/19389879

[5] ttp://www.medscape.com/viewarticle/573902_4

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[2]

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 [[AC220]] and [[midostaurin]] are in phase II clinical trials for AML patients with FLT3 mutations.<ref>http://clinicaltrials.gov/ct2/show/NCT00989261 "Efficacy Study for AC220 to Treat Acute Myeloid Leukemia (AML) (ACE)"</ref><ref>http://www.genengnews.com/news/bnitem.aspx?name=71385927 "Astellas Pays $40M Up Front to Develop Ambit’s FLT3 Kinase Inhibitors"</ref>
+[[Sorafenib]] has been reported to show significant activity against Flt3-ITD positive [[acute myelogenous leukemia]].<ref>http://www.ncbi.nlm.nih.gov/pubmed/19389879</ref><ref>http://www.medscape.com/viewarticle/573902_4</ref>
 ==See also==

v t e Proteins: clusters of differentiation (see also list of human clusters of differentiation)
1–50	CD1 a-c 1A 1B 1D 1E CD2 CD3 γ δ ε CD4 CD5 CD6 CD7 CD8 a CD9 CD10 CD11 a b c d CD13 CD14 CD15 CD16 A B CD18 CD19 CD20 CD21 CD22 CD23 CD24 CD25 CD26 CD27 CD28 CD29 CD30 CD31 CD32 A B CD33 CD34 CD35 CD36 CD37 CD38 CD39 CD40 CD41 CD42 a b c d CD43 CD44 CD45 CD46 CD47 CD48 CD49 a b c d e f CD50
51–100	CD51 CD52 CD53 CD54 CD55 CD56 CD57 CD58 CD59 CD61 CD62 E L P CD63 CD64 A B C CD66 a b c d e f CD68 CD69 CD70 CD71 CD72 CD73 CD74 CD78 CD79 a b CD80 CD81 CD82 CD83 CD84 CD85 a d e h j k CD86 CD87 CD88 CD89 CD90 CD91 - CD92 CD93 CD94 CD95 CD96 CD97 CD98 CD99 CD100
101–150	CD101 CD102 CD103 CD104 CD105 CD106 CD107 a b CD108 CD109 CD110 CD111 CD112 CD113 CD114 CD115 CD116 CD117 CD118 CD119 CD120 a b CD121 a b CD122 CD123 CD124 CD125 CD126 CD127 CD129 CD130 CD131 CD132 CD133 CD134 CD135 CD136 CD137 CD138 CD140b CD141 CD142 CD143 CD144 CD146 CD147 CD148 CD150
151–200	CD151 CD152 CD153 CD154 CD155 CD156 a b c CD157 CD158 (a d e i k) CD159 a c CD160 CD161 CD162 CD163 CD164 CD166 CD167 a b CD168 CD169 CD170 CD171 CD172 a b g CD174 CD177 CD178 CD179 a b CD180 CD181 CD182 CD183 CD184 CD185 CD186 CD191 CD192 CD193 CD194 CD195 CD196 CD197 CDw198 CDw199 CD200
201–250	CD201 CD202b CD204 CD205 CD206 CD207 CD208 CD209 CDw210 a b CD212 CD213a 1 2 CD217 CD218 (a b) CD220 CD221 CD222 CD223 CD224 CD225 CD226 CD227 CD228 CD229 CD230 CD233 CD234 CD235 a b CD236 CD238 CD239 CD240CE CD240D CD241 CD243 CD244 CD246 CD247 - CD248 CD249
251–300	CD252 CD253 CD254 CD256 CD257 CD258 CD261 CD262 CD263 CD264 CD265 CD266 CD267 CD268 CD269 CD271 CD272 CD273 CD274 CD275 CD276 CD278 CD279 CD280 CD281 CD282 CD283 CD284 CD286 CD288 CD289 CD290 CD292 CDw293 CD294 CD295 CD297 CD298 CD299
301–350	CD300A CD301 CD302 CD303 CD304 CD305 CD306 CD307 CD309 CD312 CD314 CD315 CD316 CD317 CD318 CD320 CD321 CD322 CD324 CD325 CD326 CD327 CD328 CD329 CD331 CD332 CD333 CD334 CD335 CD336 CD337 CD338 CD339 CD340 CD344 CD349 CD350