SDHD succinate dehydrogenase complex, subunit D, integral membrane protein [Homo sapiens (human)] - Gene

Summary

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Official Symbol: SDHDprovided by HGNC
Official Full Name: succinate dehydrogenase complex, subunit D, integral membrane proteinprovided by HGNC
Primary source: HGNC:10683
See related: Ensembl:ENSG00000204370; HPRD:04069; MIM:602690; Vega:OTTHUMG00000166997
Gene type: protein coding
RefSeq status: REVIEWED
Organism: Homo sapiens
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo
Also known as: PGL; CBT1; CWS3; PGL1; QPs3; SDH4; cybS; CII-4
Summary: This gene encodes a member of complex II of the respiratory chain, which is responsible for the oxidation of succinate. The encoded protein is one of two integral membrane proteins anchoring the complex to the matrix side of the mitochondrial inner membrane. Mutations in this gene are associated with the formation of tumors, including hereditary paraganglioma. Transmission of disease occurs almost exclusively through the paternal allele, suggesting that this locus may be maternally imprinted. There are pseudogenes for this gene on chromosomes 1, 2, 3, 7, and 18. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Feb 2013]

Genomic context

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Location :: 11q23

Sequence :: Chromosome: 11; NC_000011.9 (111957571..111966518)

See SDHD in Epigenomics, MapViewer

Chromosome 11 - NC_000011.9 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence

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Bibliography

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GeneRIFs: Gene References Into Functions What's a GeneRIF?

The high prevalence of the G12S polymorphism of the SDHD gene in patients with multiple endocrine neoplasia type 2A raises questions about its role as a genetic modifier, but this proposal remains to be established.
Title: Over-representation of the G12S polymorphism of the SDHD gene in patients with MEN2A syndrome.
In paraganglioma, 10 different SDHD mutations were detected.
Title: Prevalence and spectrum of SDHx mutations in pheochromocytoma and paraganglioma in patients from Belgium: an update.
Tumor DNA mutation screening of the SDHx, VHL, and RET genes and LOH analyses of the SDHx and VHL genes were performed for pheochromocytoma.
Title: Somatic mutation analysis of the SDHB, SDHC, SDHD, and RET genes in the clinical assessment of sporadic and hereditary pheochromocytoma.
No mutations were found in SDHD gene in cases of pheochromocytoma and abdominal paraganglioma in Western Sweden.
Title: Prevalence of germline mutations in patients with pheochromocytoma or abdominal paraganglioma and sporadic presentation: a population-based study in Western Sweden.
Description of the first kindred with a germline SDHD pathogenic mutation, inherited paragangliomas, and acromegaly due to a GH-producing pituitary adenoma.
Title: Succinate dehydrogenase (SDH) D subunit (SDHD) inactivation in a growth-hormone-producing pituitary tumor: a new association for SDH?
two mis-sense mutations at the start codon of the SDHD gene, including p.Met1Val (c.1A>G) and p.Met1Ile (c.3G>C), might be mutation hotspots in Chinese patients with familial Head and neck paragangliomas
Title: Common genetic mutations in the start codon of the SDH subunit D gene among Chinese families with familial head and neck paragangliomas.
Combination of demographic/geographical/historical conditions in Trentino, Italy, resulted in oldest/largest SDHD founder effect so far characterized and has transformed a rare disease (paraganglioma syndrome type 1) into an endemic disease.
Title: The endemic paraganglioma syndrome type 1: origin, spread, and clinical expression.
The results provide molecular evidence for imprinting at a boundary element flanking the SDHD locus and suggest that epigenetic suppression of the maternal allele is the underlying mechanism of the imprinted penetrance of SDHD mutations.
Title: Genomic imprinting at a boundary element flanking the SDHD locus.
The large majority of the patients carried mutations in SDHD (83%), and the p.Asp92Tyr Dutch founder mutation in SDHD alone accounted for 72% of all patients with HNPGL.
Title: Mutations in SDHD are the major determinants of the clinical characteristics of Dutch head and neck paraganglioma patients.
pheochromocytoma formation can occur after maternal transmission of SDHD;tumor formation in SDHD mutation requires loss of wild-type SDHD allele and maternal 11p15 leading to predominant but not exclusive inheritance pattern after paternal SDHD transm
Title: Molecular analysis of pheochromocytoma after maternal transmission of SDHD mutation elucidates mechanism of parent-of-origin effect.

Submit: New GeneRIF Correction See all (60)

Phenotypes

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Find tests for this gene in the NIH Genetic Testing Registry (GTR)

Review eQTL and phenotype association data in this region using PheGenI

Paraganglioma and gastric stromal sarcoma

MIM: 606864

Genetic Testing Registry

Hereditary paraganglioma-pheochromocytoma (PGL/PCC) syndromes are characterized by paragangliomas (tumors that arise from neuroendocrine tissues symmetrically distributed along the paravertebral axis from the base of the skull to the pelvis) and by pheochromocytomas (paragangliomas that are confined to the adrenal medulla). Sympathetic paragangliomas hypersecrete catecholamines; parasympathetic paragangliomas are most often nonsecretory. Extra-adrenal parasympathetic paragangliomas are located predominantly in the skull base, neck, and upper medistinum; approximately 95% of such tumors are nonsecretory. In contrast, sympathetic extra-adrenal paragangliomas are generally confined to the lower mediastinum, abdomen, and pelvis, and are typically secretory. Pheochromocytomas, which arise from the adrenal medulla, typically hypersecrete catecholamines. Symptoms of PGL/PCC result either from mass effects or catecholamine hypersecretion (e.g., sustained or paroxysmal elevations in blood pressure, headache, episodic profuse sweating, forceful palpitations, pallor, and apprehension or anxiety). The risk for malignant transformation is greater for extra-adrenal sympathetic paragangliomas than for pheochromocytomas or skull base and neck paragangliomas.

Diagnosis Testing

The diagnosis of hereditary PGL/PCC syndromes is based on physical examination, family history, imaging studies, biochemical testing, and molecular genetic testing. SDHA, SDHB, SDHC and SDHD are four nuclear genes that encode the four subunits of the mitochondrial enzyme succinate dehydrogenase (SDH). A fifth nuclear gene, SDHAF2 (also known as SDH5) encodes a protein that appears to be required for flavination of another SDH subunit, SDHA. These are collectively known as the SDHx genes. Mutations in MAX predispose to PCC; a subset of individuals with mutations in MAX will also develop PGL. KIF1B and EGLN1 (formerly known as PHD2) have been reported to be associated with hereditary PGL/PCC, but their clinical significance is still unclear. Molecular genetic testing for disease-causing variants in SDHA, SDHB, SDHC, SDHD, SDHAF2, and MAX is clinically available.

Genetic Counseling

The hereditary PGL/PCC syndromes are inherited in an autosomal dominant manner. Mutations in SDHD (PGL1) demonstrate parent-of-origin effects and generally cause disease only when the mutation is inherited from the father. Initial data suggest that mutations in SDHAF2 (PGL2) and MAX exhibit parent-of-origin effects similar to those of mutations in SDHD. A proband with a hereditary PGL/PCC syndrome may have inherited the mutation from a parent or have a de novo mutation; the proportion of cases caused by de novo mutations is unknown. Each child of an individual with a hereditary PGL/PCC syndrome has a 50% chance of inheriting the disease-causing mutation. An individual who inherits a SDHD mutation from his/her mother is at a low but not negligible risk of developing disease; each of his/her offspring is at a 50% risk of inheriting the disease-causing allele. An individual who inherits an SDHD mutation from his/her father is at high risk of manifesting paragangliomas and, to a lesser extent, pheochromocytomas. Prenatal testing for pregnancies at increased risk is possible for families in which the disease-causing mutation is known; if no laboratories offering prenatal testing are listed in the GeneTeststrade mark Laboratory Directory, such testing may be available through laboratories offering custom prenatal testing.

References

PMID: 20301715

Pheochromocytoma

MIM: 171300

Genetic Testing Registry

Summary from GeneReviews: Hereditary Paraganglioma-Pheochromocytoma Syndromes

Disease Characteristics

Hereditary paraganglioma-pheochromocytoma (PGL/PCC) syndromes are characterized by paragangliomas (tumors that arise from neuroendocrine tissues symmetrically distributed along the paravertebral axis from the base of the skull to the pelvis) and by pheochromocytomas (paragangliomas that are confined to the adrenal medulla). Sympathetic paragangliomas hypersecrete catecholamines; parasympathetic paragangliomas are most often nonsecretory. Extra-adrenal parasympathetic paragangliomas are located predominantly in the skull base, neck, and upper medistinum; approximately 95% of such tumors are nonsecretory. In contrast, sympathetic extra-adrenal paragangliomas are generally confined to the lower mediastinum, abdomen, and pelvis, and are typically secretory. Pheochromocytomas, which arise from the adrenal medulla, typically hypersecrete catecholamines. Symptoms of PGL/PCC result either from mass effects or catecholamine hypersecretion (e.g., sustained or paroxysmal elevations in blood pressure, headache, episodic profuse sweating, forceful palpitations, pallor, and apprehension or anxiety). The risk for malignant transformation is greater for extra-adrenal sympathetic paragangliomas than for pheochromocytomas or skull base and neck paragangliomas.

Diagnosis Testing

The diagnosis of hereditary PGL/PCC syndromes is based on physical examination, family history, imaging studies, biochemical testing, and molecular genetic testing. SDHA, SDHB, SDHC and SDHD are four nuclear genes that encode the four subunits of the mitochondrial enzyme succinate dehydrogenase (SDH). A fifth nuclear gene, SDHAF2 (also known as SDH5) encodes a protein that appears to be required for flavination of another SDH subunit, SDHA. These are collectively known as the SDHx genes. Mutations in MAX predispose to PCC; a subset of individuals with mutations in MAX will also develop PGL. KIF1B and EGLN1 (formerly known as PHD2) have been reported to be associated with hereditary PGL/PCC, but their clinical significance is still unclear. Molecular genetic testing for disease-causing variants in SDHA, SDHB, SDHC, SDHD, SDHAF2, and MAX is clinically available.

Genetic Counseling

The hereditary PGL/PCC syndromes are inherited in an autosomal dominant manner. Mutations in SDHD (PGL1) demonstrate parent-of-origin effects and generally cause disease only when the mutation is inherited from the father. Initial data suggest that mutations in SDHAF2 (PGL2) and MAX exhibit parent-of-origin effects similar to those of mutations in SDHD. A proband with a hereditary PGL/PCC syndrome may have inherited the mutation from a parent or have a de novo mutation; the proportion of cases caused by de novo mutations is unknown. Each child of an individual with a hereditary PGL/PCC syndrome has a 50% chance of inheriting the disease-causing mutation. An individual who inherits a SDHD mutation from his/her mother is at a low but not negligible risk of developing disease; each of his/her offspring is at a 50% risk of inheriting the disease-causing allele. An individual who inherits an SDHD mutation from his/her father is at high risk of manifesting paragangliomas and, to a lesser extent, pheochromocytomas. Prenatal testing for pregnancies at increased risk is possible for families in which the disease-causing mutation is known; if no laboratories offering prenatal testing are listed in the GeneTeststrade mark Laboratory Directory, such testing may be available through laboratories offering custom prenatal testing.

References

PMID: 20301715

Pathways from BioSystems

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Alzheimer's disease, organism-specific biosystem (from KEGG)
Alzheimer's disease, organism-specific biosystemAlzheimer's disease (AD) is a chronic disorder that slowly destroys neurons and causes serious cognitive disability. AD is associated with senile plaques and neurofibrillary tangles (NFTs). Amyloid-b...
Alzheimer's disease, conserved biosystem (from KEGG)
Alzheimer's disease, conserved biosystemAlzheimer's disease (AD) is a chronic disorder that slowly destroys neurons and causes serious cognitive disability. AD is associated with senile plaques and neurofibrillary tangles (NFTs). Amyloid-b...
Citrate cycle (TCA cycle), organism-specific biosystem (from KEGG)
Citrate cycle (TCA cycle), organism-specific biosystemThe citrate cycle (TCA cycle, Krebs cycle) is an important aerobic pathway for the final steps of the oxidation of carbohydrates and fatty acids. The cycle starts with acetyl-CoA, the activated form ...
Citrate cycle (TCA cycle), conserved biosystem (from KEGG)
Citrate cycle (TCA cycle), conserved biosystemThe citrate cycle (TCA cycle, Krebs cycle) is an important aerobic pathway for the final steps of the oxidation of carbohydrates and fatty acids. The cycle starts with acetyl-CoA, the activated form ...
Citrate cycle, second carbon oxidation, 2-oxoglutarate => oxaloacetate, organism-specific biosystem (from KEGG)
Citrate cycle, second carbon oxidation, 2-oxoglutarate => oxaloacetate, organism-specific biosystemPathway module; Carbohydrate and lipid metabolism; Central carbohydrate metabolism
Citrate cycle, second carbon oxidation, 2-oxoglutarate => oxaloacetate, conserved biosystem (from KEGG)
Citrate cycle, second carbon oxidation, 2-oxoglutarate => oxaloacetate, conserved biosystemPathway module; Carbohydrate and lipid metabolism; Central carbohydrate metabolism
Citric acid cycle (TCA cycle), organism-specific biosystem (from REACTOME)
Citric acid cycle (TCA cycle), organism-specific biosystemIn the citric acid or tricarboxylic acid (TCA) cycle, the acetyl group of acetyl CoA (derived primarily from oxidative decarboxylation of pyruvate, beta-oxidation of long-chain fatty acids, and catab...
Electron Transport Chain, organism-specific biosystem (from WikiPathways)
Electron Transport Chain, organism-specific biosystemAn electron transport chain(ETC) couples a chemical reaction between an electron donor (such as NADH) and an electron acceptor (such as O2) to the transfer of H+ ions across a membrane, through a set...
Huntington's disease, organism-specific biosystem (from KEGG)
Huntington's disease, organism-specific biosystemHuntington disease (HD) is an autosomal-dominant neurodegenerative disorder that primarily affects medium spiny striatal neurons (MSN). The symptoms are choreiform, involuntary movements, personality...
Huntington's disease, conserved biosystem (from KEGG)
Huntington's disease, conserved biosystemHuntington disease (HD) is an autosomal-dominant neurodegenerative disorder that primarily affects medium spiny striatal neurons (MSN). The symptoms are choreiform, involuntary movements, personality...
Metabolism, organism-specific biosystem (from REACTOME)
Metabolism, organism-specific biosystemMetabolic processes in human cells generate energy through the oxidation of molecules consumed in the diet and mediate the synthesis of diverse essential molecules not taken in the diet as well as th...
Oxidative phosphorylation, organism-specific biosystem (from KEGG)
Oxidative phosphorylation, organism-specific biosystem
Oxidative phosphorylation
Oxidative phosphorylation, conserved biosystem (from KEGG)
Oxidative phosphorylation, conserved biosystem
Oxidative phosphorylation
Parkinson's disease, organism-specific biosystem (from KEGG)
Parkinson's disease, organism-specific biosystemParkinson's disease (PD) is a progressive neurodegenerative movement disorder that results primarily from the death of dopaminergic neurons in the substantia nigra. Mutations in alpha-synuclein, UCHL...
Pyruvate metabolism and Citric Acid (TCA) cycle, organism-specific biosystem (from REACTOME)
Pyruvate metabolism and Citric Acid (TCA) cycle, organism-specific biosystemPyruvate metabolism and the citric acid (TCA) cycle together link the processes of energy metabolism in a human cell with one another and with key biosynthetic reactions. Pyruvate, derived from the r...
Respiratory electron transport, organism-specific biosystem (from REACTOME)
Respiratory electron transport, organism-specific biosystemMitochondria are often described as the "powerhouse" of a cell as it is here that energy is largely released from the oxidation of food. Reducing equivalents generated from beta-oxidation of fatty ac...
Respiratory electron transport, ATP synthesis by chemiosmotic coupling, and heat production by uncoupling proteins., organism-specific biosystem (from REACTOME)
Respiratory electron transport, ATP synthesis by chemiosmotic coupling, and heat production by uncoupling proteins., organism-specific biosystemOxidation of fatty acids and pyruvate in the mitochondrial matrix yield large amounts of NADH. The respiratory electron transport chain couples the re-oxidation of this NADH to NAD+ to the export of ...
Succinate dehydrogenase (ubiquinone), organism-specific biosystem (from KEGG)
Succinate dehydrogenase (ubiquinone), organism-specific biosystemStructural complex; Energy metabolism; ATP synthesis
TCA Cycle, organism-specific biosystem (from WikiPathways)
TCA Cycle, organism-specific biosystemThe [[wikipedia:citric_acid_cycle|citric acid cycle]], also known as the tricarboxylic acid cycle (TCA cycle) or the Krebs cycle, (or rarely, the Szent-Gyorgyi-Krebs cycle) is a series of enzyme-cata...
TCA cycle, organism-specific biosystem (from BIOCYC)
TCA cycle, organism-specific biosystem
TCA cycle
TCA cycle II (eukaryotic), conserved biosystem (from BIOCYC)
TCA cycle II (eukaryotic), conserved biosystemGeneral Background The TCA pathway is a catabolic pathway of aerobic respiration that generates both energy and reducing power. In addition, it is also the first step in generating precursors for bi...
The citric acid (TCA) cycle and respiratory electron transport, organism-specific biosystem (from REACTOME)
The citric acid (TCA) cycle and respiratory electron transport, organism-specific biosystemThe metabolism of pyruvate provides one source of acetyl-CoA which enters the citric acid (TCA, tricarboxylic acid) cycle to generate energy and the reducing equivalent NADH. These reducing equivalen...

General gene information

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Markers

D11S2246E (e-PCR)
- UniSTS:151407

RH80714 (e-PCR)
- UniSTS:91505

RH64925 (e-PCR)
- UniSTS:49069

A002R25 (e-PCR)
- UniSTS:56503

WI-11979 (e-PCR)
- UniSTS:80122

Genotypes

See SDHD SNP Geneview Report
See SDHD SNP Genotype Report
See SDHD SNP Variation Viewer Report

Related pseudogene(s)

7 found Review record(s) in Gene

Potential readthrough

Included genes: TEX12, BCO2

Homology

Homologs of the SDHD gene: The SDHD gene is conserved in chimpanzee, Rhesus monkey, dog, cow, mouse, rat, chicken, zebrafish, fruit fly, and mosquito.
Map Viewer (Mouse, Rat)
OrthoDB: The Hierarchical Catalog of Eukaryotic Orthologs

Gene Ontology Provided by GOA

Function	Evidence Code	Pubs
electron carrier activity	TAS Traceable Author Statement more info	PubMed
heme binding	ISS Inferred from Sequence or Structural Similarity more info
metal ion binding	IEA Inferred from Electronic Annotation more info
succinate dehydrogenase activity	IDA Inferred from Direct Assay more info	PubMed
ubiquinone binding	ISS Inferred from Sequence or Structural Similarity more info

Process	Evidence Code	Pubs
respiratory electron transport chain	TAS Traceable Author Statement more info
small molecule metabolic process	TAS Traceable Author Statement more info
tricarboxylic acid cycle	IDA Inferred from Direct Assay more info	PubMed
tricarboxylic acid cycle	IEA Inferred from Electronic Annotation more info
tricarboxylic acid cycle	TAS Traceable Author Statement more info

Component	Evidence Code	Pubs
integral to membrane	IEA Inferred from Electronic Annotation more info
mitochondrial envelope	TAS Traceable Author Statement more info	PubMed
mitochondrial inner membrane	IDA Inferred from Direct Assay more info	PubMed
mitochondrial inner membrane	ISS Inferred from Sequence or Structural Similarity more info
mitochondrial inner membrane	TAS Traceable Author Statement more info
mitochondrial respiratory chain complex II	ISS Inferred from Sequence or Structural Similarity more info
mitochondrion	TAS Traceable Author Statement more info	PubMed

General protein information

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Preferred Names: succinate dehydrogenase [ubiquinone] cytochrome b small subunit, mitochondrial

Names: succinate dehydrogenase [ubiquinone] cytochrome b small subunit, mitochondrial; succinate-ubiquinone reductase membrane anchor subunit; succinate-ubiquinone oxidoreductase cytochrome b small subunit

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.

Genomic

NG_012337.2 RefSeqGene

Range

4978..13955

Download

GenBank, FASTA, Sequence Viewer (Graphics)

mRNA and Protein(s)

NM_001276503.1 → NP_001263432.1 succinate dehydrogenase [ubiquinone] cytochrome b small subunit, mitochondrial isoform b precursor

Status: REVIEWED

Description

Transcript Variant: This variant (2) lacks an alternate coding exon, which results in a frameshift, compared to variant 1. The encoded isoform (b) is shorter and has a distinct C-terminus, compared to isoform a.

Source sequence(s)

AI753083, AP002007, BC015188, BQ932668, CD105572

UniProtKB/TrEMBL

E9PQI9
NM_001276504.1 → NP_001263433.1 succinate dehydrogenase [ubiquinone] cytochrome b small subunit, mitochondrial isoform c precursor

Status: REVIEWED

Description

Transcript Variant: This variant (3) lacks an alternate coding exon, but retains the reading frame, compared to variant 1. The encoded isoform (c) is shorter than isoform a.

Source sequence(s)

AI753083, AP002007, BC015188, BF211358, BQ932668

UniProtKB/TrEMBL

E9PIC0

Conserved Domains (1) summary

cl00881
Location:18 – 119
Blast Score: 225

SQR_QFR_TM; Succinate:quinone oxidoreductase (SQR) and Quinol:fumarate reductase (QFR) family, transmembrane subunits; SQR catalyzes the oxidation of succinate to fumarate coupled to the reduction of quinone to quinol, while QFR catalyzes the reverse reaction. SQR, ...
NM_001276506.1 → NP_001263435.1 succinate dehydrogenase [ubiquinone] cytochrome b small subunit, mitochondrial isoform d precursor

Status: REVIEWED

Description

Transcript Variant: This variant (4) contains an alternate coding exon, which results in a frameshift, compared to variant 1. The encoded isoform (d) is shorter and has a distinct C-terminus, compared to isoform a.

Source sequence(s)

AI753083, AP002007, BC015188, BG492859, BQ932668

UniProtKB/TrEMBL

E9PIG3

Conserved Domains (1) summary

cl00881
Location:57 – 105
Blast Score: 122

SQR_QFR_TM; Succinate:quinone oxidoreductase (SQR) and Quinol:fumarate reductase (QFR) family, transmembrane subunits; SQR catalyzes the oxidation of succinate to fumarate coupled to the reduction of quinone to quinol, while QFR catalyzes the reverse reaction. SQR, ...
NM_003002.3 → NP_002993.1 succinate dehydrogenase [ubiquinone] cytochrome b small subunit, mitochondrial isoform a precursor

Status: REVIEWED

Description

Transcript Variant: This variant (1) encodes the longest isoform (a).

Source sequence(s)

AI753083, AP002007, BC015188, BQ932668

Consensus CDS

CCDS31678.1

UniProtKB/Swiss-Prot

O14521

Related

ENSP00000364699, OTTHUMP00000234720, ENST00000375549, OTTHUMT00000392351

Conserved Domains (1) summary

cd03496
Location:60 – 158
Blast Score: 225

SQR_TypeC_CybS; SQR catalyzes the oxidation of succinate to fumarate coupled to the reduction of quinone to quinol. Eukaryotic SQRs reduce high potential quinones such as ubiquinone. SQR is also called succinate dehydrogenase or Complex II, and is part of the citric ...

RNA

NR_077060.1 RNA Sequence

Status: REVIEWED

Description

Transcript Variant: This variant (5) contains an alternate internal exon, compared to variant 1. This variant is represented as non-coding because the use of the translational start codon, as used in variant 1, renders the transcript a candidate for nonsense-mediated mRNA decay (NMD).

Source sequence(s)

AI753083, AP002007, BC015188, BE567994, BQ932668

RefSeqs of Annotated Genomes: Homo sapiens Annotation Release 104

The following sections contain reference sequences that belong to a specific genome build. Explain

Reference GRCh37.p10 Primary Assembly

Genomic

NC_000011.9 Reference GRCh37.p10 Primary Assembly

Range

111957571..111966518

Download

GenBank, FASTA, Sequence Viewer (Graphics)

Alternate HuRef

Genomic

AC_000143.1 Alternate HuRef

Range

107881603..107890550

Download

GenBank, FASTA, Sequence Viewer (Graphics)

Alternate CHM1_1.0

Genomic

NC_018922.1 Alternate CHM1_1.0

Range

111821039..111829987

Download

GenBank, FASTA, Sequence Viewer (Graphics)

Nucleotide		Protein
Heading	Accession and Version	Protein
genomic	AB026906.1	BAA81889.1
genomic	ABBA01039805.1 (39395..48342)	None
genomic	AMYH01004034.1 (28135..37083)	None
genomic	AP002007.4 (103917..112894)	None
genomic	CH471065.1	EAW67181.1
		EAW67182.1
		EAW67183.1
mRNA	AA374642.1	None
mRNA	AB006202.1	BAA22054.1
mRNA	AI753083.1	None
mRNA	AK075360.1	BAG52120.1
mRNA	BC005263.1	AAH05263.1
mRNA	BC009574.1	AAH09574.1
mRNA	BC012603.1	AAH12603.1
mRNA	BC015188.1	AAH15188.1
mRNA	BC015992.1	AAH15992.1
mRNA	BC022350.1	AAH22350.1
mRNA	BC070307.1	AAH70307.1
mRNA	BC071755.1	AAH71755.1
mRNA	BC071756.1	AAH71756.1
mRNA	BE567994.1	None
mRNA	BF211358.1	None
mRNA	BG492859.1	None
mRNA	BQ000657.1	None
mRNA	BQ932668.1	None
mRNA	BT007238.1	AAP35902.1
mRNA	BX419391.2	None
mRNA	CD105572.1	None
mRNA	CR456932.1	CAG33213.1
other-genetic	DQ892701.2	ABM83627.1
other-genetic	DQ896292.2	ABM87291.1