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Protein Page:
ALDOB (human)
p Phosphorylation
a Acetylation
m Methylation
m1 Mono-methylation
m2 Di-methylation
m3 Tri-methylation
u Ubiquitination
s Sumoylation
n Neddylation
gl O-GlcNAc
ga O-GalNAc
h Palmitoylation
ad Adenylylation
sn S-Nitrosylation
ca Caspase cleavage

Overview
ALDOB Defects in ALDOB are the cause of hereditary fructose intolerance (HFI). HFI is an autosomal recessive disease that results in an inability to metabolize fructose and related sugars. Complete exclusion of fructose results in dramatic recovery; however, if not treated properly, HFI subjects suffer episodes of hypoglycemia, general ill condition, and risk of death the remainder of life. Belongs to the class I fructose-bisphosphate aldolase family. Note: This description may include information from UniProtKB.
Protein type: EC 4.1.2.13; Lyase; Carbohydrate Metabolism - glycolysis and gluconeogenesis; Carbohydrate Metabolism - pentose phosphate pathway; Carbohydrate Metabolism - fructose and mannose
Cellular Component: microtubule organizing center; cytosol
Molecular Function: identical protein binding; protein binding; cytoskeletal protein binding; fructose-bisphosphate aldolase activity; ATPase binding
Biological Process: fructose 1,6-bisphosphate metabolic process; NADH oxidation; glycolysis; positive regulation of ATPase activity; carbohydrate metabolic process; glucose metabolic process; fructose catabolic process; fructose metabolic process; gluconeogenesis
Reference #:  P05062 (UniProtKB)
Alt. Names/Synonyms: ALDB; ALDO2; ALDOB; aldolase 2; aldolase B, fructose-bisphosphatase; aldolase B, fructose-bisphosphate; Fructose-bisphosphate aldolase B; Liver-type aldolase
Gene Symbols: ALDOB
Molecular weight: 39,473 Da
Basal Isoelectric point: 8.01  Predict pI for various phosphorylation states
Select Structure to View Below

ALDOB

Protein Structure Not Found.


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Modification Sites and Domains Show Modification Legend
Click here to view phosphorylation modifications only

Modification Sites in Parent Protein, Orthologs, and Isoforms Show Modification Legend
 

Show Multiple Sequence Alignment


 SS 

SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.


 MS 

MS: The number of records in which this modification site was assigned using ONLY proteomic discovery-mode mass spectrometry.


       human

 
0 1 K14 ALTQEQKKELSEIAQ
0 1 K14 ALTQEQKKELSEIAQ
0 1 K28 QSIVANGKGILAADE
0 5 S36-p GILAADEsVGtMGNR
0 5 T39-p AADEsVGtMGNRLQR
0 2 K48 GNRLQRIKVENTEEN
0 1 K101 FRNILKEKGIVVGIK
0 1 K108 KGIVVGIKLDQGGAP
0 2 K108 KGIVVGIKLDQGGAP
0 1 K121 APLAGTNKEttIQGL
0 2 K121 APLAGTNKEttIQGL
0 2 T123-p LAGTNKEttIQGLDG
0 2 T124-p AGTNKEttIQGLDGL
0 9 K139-a SERCAQYkKDGVDFG
0 1 K140 ERCAQYkKDGVDFGk
0 8 K147-a KDGVDFGkWRAVLRI
0 1 K147 KDGVDFGKWRAVLRI
0 1 S161 IADQCPSSLAIQENA
0 154 Y204-p HDLEHCQyVtEkVLA
0 8 T206-p LEHCQyVtEkVLAAV
0 2 K208-a HCQyVtEkVLAAVYK
0 28 K208-u HCQyVtEkVLAAVYK
0 10 Y223-p ALNDHHVyLEGTLLK
0 1 K230 yLEGTLLKPNMVTAG
0 1 K230 yLEGTLLKPNMVTAG
0 7 K242-a TAGHACTkkYTPEQV
0 1 K242 TAGHACTKkYTPEQV
0 3 K243-a AGHACTkkYTPEQVA
0 1 K243 AGHACTkKYTPEQVA
0 1 S272 VPGICFLSGGMSEED
0 8 Y302-p PWKLSFSyGRALQAS
0 1 K317 ALAAWGGKAANKEAT
0 1 E322 GGKAANKEATQEAFM
0 6 K330-a ATQEAFMkRAMANCQ
0 2 K330 ATQEAFMKRAMANCQ
1 1 Y362-p QSLFTACyTY_____
  mouse

 
K14-a ALTPEQKkELSEIAQ
K14-u ALTPEQKkELSEIAQ
K28-u QRIVANGkGILAADE
S36-p GILAADEsVGtMGNR
T39-p AADEsVGtMGNRLQR
K48-u GNRLQRIkVENTEEN
K101-u FRNVLKEkGIVVGIk
K108-a kGIVVGIkLDQGGAP
K108-u kGIVVGIkLDQGGAP
K121-a APLAGTNkETTIQGL
K121-u APLAGTNkETTIQGL
T123 LAGTNkETTIQGLDG
T124 AGTNkETTIQGLDGL
K139-a SERCAQYkkDGVDFG
K140-u ERCAQYkkDGVDFGk
K147-a kDGVDFGkWRAVLRI
K147-u kDGVDFGkWRAVLRI
S161-p IADQCPSsLAIQENA
Y204-p HDLEHCQyVsEKVLA
S206-p LEHCQyVsEKVLAAV
K208 HCQyVsEKVLAAVYK
K208 HCQyVsEKVLAAVYK
Y223-p ALNDHHVyLEGTLLk
K230-a yLEGTLLkPNMVTAG
K230-u yLEGTLLkPNMVTAG
K242-a TAGHACTkkYTPEQV
K242-u TAGHACTkkYTPEQV
K243 AGHACTkKYTPEQVA
K243-u AGHACTkkYTPEQVA
S272-p VPGICFLsGGMSEED
Y302 PWKLSFSYGRALQAS
K317-u ALAAWGGkAANKkAT
K322-u GGkAANKkATQEAFM
K330-a ATQEAFMkRAMANCQ
K330-u ATQEAFMkRAMANCQ
Y362 QSLFTASYTY_____
  rat

 
K14 ALTSEQKKELSEIAQ
K14 ALTSEQKKELSEIAQ
K28 QRIVANGKGILAADE
S36-p GILAADEsVGtMGNR
T39-p AADEsVGtMGNRLQR
K48 GNRLQRIKVENTEEN
K101 FRNILKEKGIVVGIK
K108 KGIVVGIKLDQGGAP
K108 KGIVVGIKLDQGGAP
K121 APLAGTNKETTIQGL
K121 APLAGTNKETTIQGL
T123 LAGTNKETTIQGLDG
T124 AGTNKETTIQGLDGL
K139 SERCAQYKKDGVDFG
K140 ERCAQYKKDGVDFGK
K147 KDGVDFGKWRAVLRI
K147 KDGVDFGKWRAVLRI
S161-p ISDQCPSsLAIQENA
Y204 HDLEHCQYVSEKVLA
S206 LEHCQYVSEKVLAAV
K208 HCQYVSEKVLAAVYK
K208 HCQYVSEKVLAAVYK
Y223 ALNDHHVYLEGTLLK
K230 YLEGTLLKPNMLTAG
K230 YLEGTLLKPNMLTAG
K242 TAGHACTKKYTPEQV
K242 TAGHACTKKYTPEQV
K243 AGHACTKKYTPEQVA
K243 AGHACTKKYTPEQVA
S272 VPSICFLSGGMSEED
Y302 PWKLSFSYGRALQAS
K317 ALAAWGGKAANKKAT
K322 GGKAANKKATQEAFM
K330 ATQEAFMKRAVANCQ
K330 ATQEAFMKRAVANCQ
Y362 QSLFTASYTY_____
  rabbit

 
K14 ALTPEQKKELSDIAQ
K14 ALTPEQKKELSDIAQ
K28 QRIVANGKGILAADE
S36 GILAADESVGTMGNR
T39 AADESVGTMGNRLQR
K48 GNRLQRIKVENTEEN
K101 FRNILKEKGIVVGIK
K108 KGIVVGIKLDQGGAP
K108 KGIVVGIKLDQGGAP
K121 APLAGTNKETTIQGL
K121 APLAGTNKETTIQGL
T123 LAGTNKETTIQGLDG
T124 AGTNKETTIQGLDGL
K139 SERCAQYKKDGVDFG
K140 ERCAQYKKDGVDFGK
K147 KDGVDFGKWRAVLRI
K147 KDGVDFGKWRAVLRI
S161 IADQCPSSLAIQENA
Y204 HDLEHCQYVTEKVLA
T206 LEHCQYVTEKVLAAV
K208 HCQYVTEKVLAAVYK
K208 HCQYVTEKVLAAVYK
Y223 ALNDHHVYLEGTLLK
K230 YLEGTLLKPNMVTAG
K230 YLEGTLLKPNMVTAG
K242 TAGHACTKKYTPEQV
K242 TAGHACTKKYTPEQV
K243 AGHACTKKYTPEQVA
K243 AGHACTKKYTPEQVA
S272 VPGICFLSGGMSEED
Y302 PWKLSFSYGRALQAS
K317 ALAAWGGKAENKKAT
K322 GGKAENKKATQEAFM
K330 ATQEAFMKRAVVNCQ
K330 ATQEAFMKRAVVNCQ
Y362-p QSLFTASyTY_____
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