Upstream stimulatory factor gene transcriptions: Difference between revisions

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! Reals or randoms !! Promoters !! direction !! Numbers !! Strands !! Occurrences !! Averages (± 0.1)  
! Reals or randoms !! Promoters !! direction !! Numbers !! Strands !! Occurrences !! Averages (± 0.1)  
|-
|-
| Reals || UTR || negative || 0 || 2 || 0 || 0  
| Reals || UTR || negative || 19,13 || 2 || 9.5,6.5 || 9.5 ± 8.5 (--1,+-18),6.5 ± 6.5 (--0,+-13)
|-
|-
| Randoms || UTR || arbitrary negative || 0 || 10 || 0 || 0  
| Randoms || UTR || arbitrary negative || 0 || 10 || 0 || 0  
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| Randoms || Core || alternate negative || 0 || 10 || 0 || 0  
| Randoms || Core || alternate negative || 0 || 10 || 0 || 0  
|-
|-
| Reals || Core || positive || 0 || 2 || 0 || 0  
| Reals || Core || positive || 1 || 2 || 0.5 || 0.5
|-
|-
| Randoms || Core || arbitrary positive || 0 || 10 || 0 || 0
| Randoms || Core || arbitrary positive || 0 || 10 || 0 || 0
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| Randoms || Core || alternate positive || 0 || 10 || 0 || 0  
| Randoms || Core || alternate positive || 0 || 10 || 0 || 0  
|-
|-
| Reals || Proximal || negative || 0 || 2 || 0 || 0  
| Reals || Proximal || negative || 1 || 2 || 0.5 || 0.5 ± 0.5 (+-1,--0)
|-
|-
| Randoms || Proximal || arbitrary negative || 0 || 10 || 0 || 0  
| Randoms || Proximal || arbitrary negative || 0 || 10 || 0 || 0  
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| Randoms || Proximal || alternate negative || 0 || 10 || 0 || 0  
| Randoms || Proximal || alternate negative || 0 || 10 || 0 || 0  
|-
|-
| Reals || Proximal || positive || 0 || 2 || 0 || 0  
| Reals || Proximal || positive || 3 || 2 || 1.5 || 1.5 ± 1.5 (-+3,++0)
|-
|-
| Randoms || Proximal || arbitrary positive || 0 || 10 || 0 || 0  
| Randoms || Proximal || arbitrary positive || 0 || 10 || 0 || 0  
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| Randoms || Proximal || alternate positive || 0 || 10 || 0 || 0  
| Randoms || Proximal || alternate positive || 0 || 10 || 0 || 0  
|-
|-
| Reals || Distal || negative || 0 || 2 || 0 || 0
| Reals || Distal || negative || 33 || 2 || 16.5 || 16.5 ± 6.5 (--10,+-23)
|-
|-
| Randoms || Distal || arbitrary negative || 0 || 10 || 0 || 0
| Randoms || Distal || arbitrary negative || 0 || 10 || 0 || 0
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| Randoms || Distal || alternate negative || 0 || 10 || 0 || 0  
| Randoms || Distal || alternate negative || 0 || 10 || 0 || 0  
|-
|-
| Reals || Distal || positive || 0 || 2 || 0 || 0
| Reals || Distal || positive || 63 || 2 || 31.5 || 31.5 ± 13.5 (-+45,++18)
|-
|-
| Randoms || Distal || arbitrary positive || 0 || 10 || 0 || 0  
| Randoms || Distal || arbitrary positive || 0 || 10 || 0 || 0  

Revision as of 08:13, 8 March 2023

Associate Editor(s)-in-Chief: Henry A. Hoff

"A major environmental stress encountered by humans is solar UV light, which can cause skin inflammation, the induction of pro-inflammatory cytokines and skin ageing, as well as skin cancer, including the highly aggressive and increasingly common malignant melanoma (Elwood, 1996; Armstrong et al., 1997; Park and Gilchrest, 1999). The serious adverse effect of UV light on the skin has meant that humans have evolved an effective defence mechanism. In response to low levels of UV irradiation epidermal melanocytes increase the production of the pigment melanin in specialized organelles termed melanosomes (Jimbow et al., 1991). The melanosomes are transferred into surrounding keratinocytes where they act to protect against UV-induced DNA damage."[1]

"The Tyrosinase gene encodes the rate-limiting enzyme for the production of melanin and is absolutely required for pigmentation; the absence of a functional tyrosinase enzyme results in an albino phenotype. Although much of the tanning response comprises a post-translational activation of the melanosome, transcription of the Tyrosinase gene is UV responsive (Hara et al., 1994; Sturm et al., 1994; Imokawa et al., 1995, 1997; Ota et al., 1998). However, analysis of the Tyrosinase promoter (Bentley et al., 1994; Ganss et al., 1994) failed to reveal any classical UV or stress-response element. The human Tyrosinase promoter comprises an SP1 site and two E box motifs, one at the initiator, and a second, termed the M box (Lowings et al., 1992), located at –100 with respect to the transcription initiation site (Bentley et al., 1994). The E box motifs are essential for Tyrosinase promoter activity and are highly evolutionarily conserved. Numerous studies (Bentley et al., 1994; Ganss et al., 1994; Hemesath et al., 1994; Yasumoto et al., 1994; Yavuzer et al., 1995; Krylov et al., 1997) have demonstrated that the Tyrosinase initiator E box and M box elements are targets for the microphthalmia-associated basic helix–loop–helix-leucine zipper (bHLH-LZ) transcription factor Mitf (Hodgkinson et al., 1993; Hughes et al., 1993). In addition to its role in regulating pigmentation genes, [the microphthalmia-associated transcription factor] Mitf is also critically required for the development of the melanocyte (Steingrímsson et al., 1994; Opdecamp et al., 1997)."[1]

The "UV response is mediated by the ubiquitous bHLH-LZ transcription factor [upstream stimulatory factor] Usf-1, which, like Mitf, binds the conserved E box elements in the Tyrosinase promoter. The ability of Usf-1 to activate transcription is regulated by a signal transduction pathway that culminates in phosphorylation and activation of Usf-1 by the p38 stress-activated kinase."[1]

"Usf-1 and Usf-2 bind the Tyrosinase promoter in vivo."[1]

"USF comprises a combination of related ubiquitous bHLH-LZ transcription factors encoded by the Usf-1 and Usf-2 genes (Gregor et al., 1990; Sirito et al., 1992, 1994). Usf-1 and Usf-2 can form either homo- or heterodimers (Sirito et al., 1992; Viollet et al., 1996), and both are present in melanocytes and melanoma cell lines [...]."[1]

Upstream stimulating or stimulatory factors

The "expressions of [Homeobox transcript antisense intergenic RNA] HOTAIR and upstream stimulatory factor 1 (USF1) was up-regulated, but miR-148b-3p was down-regulated in glioma microvascular endothelial cells (GECs)."[2]

"Upstream stimulating factor (USF) includes upstream stimulating factor 1 (USF1) and upstream stimulating factor 2 (USF2), which belongs to the basic helix-loop-helix leucine zipper family of transcription factors. As an important regulatory factor, USF has highly conserved bHLH-LZ domain and binds to consensus sequence (CANNTG) of E-box to further regulate the transcription process of different proteins (Wu et al., 2013; Lupp et al., 2014). USF1 was reported to regulate the expression of IL-10 in glioma related microglia: inhibition of USF1 expression resulted in the up-regulation of IL-10 expression (Zhang et al., 2007). In liver cancer HepG2 cells, USF1 resisted oxygen sugar deprivation induced apoptosis by regulating miR-132 (Wang et al., 2014)."[2]

"The helix-loop-helix transcription factor USF (upstream stimulating factor) binds to a regulatory sequence of the human insulin gene enhancer."[3]

"The regulation of insulin gene expression is dependent on sequences located upstream of the transcription start site (Clark and Docherty, 1992). Two important cis-acting elements, the insulin enhancer binding site 1 (IEBI) or NIR box and the IEB2 or FAR box, have been identified in the rat insulin I gene (Karlsson et al., 1987, 1989). Located at positions -104 (IEBI/NIR) and -233 (IEB2/FAR), these elements share an identical 8 bp sequence, GCCATCTG, which contains a consensus sequence, CANNTG, characteristic of E-box elements (Kingston, 1989). E boxes are present in enhancers from a variety of genes, including immunoglobulin and muscle-specific genes, where they interact with transcription factors containing a helix-loop-helix (HLH) dimerization domain (Murre et al., 1989)."[3]

"The IEB1 box is highly conserved among insulin genes, and is thus likely to play an important role in controlling transcription. The IEB2 site is not well conserved; in the rat insulin 2 gene the equivalent sequence is GCCACCCAGGAG, and in the human insulin gene the homologous sequence, which has been previously designated the GC2 box (Boam et al., 1990a), is GCCACCGG."[3]

"Confirmation that USF bound at the IEB2 site was obtained using an oligonucleotide containing the USF binding site from the adenovirus MLP."[3]

"GCCATCTG, which contains a consensus sequence, CANNTG"[3], + "GCCACCGG."[3] which suggests GCCANN(G/T)G. Adding in a portion in the rat insulin 2 gene the equivalent sequence is GCCACCCA yields GCCANN(C/G/T)(A/G).[3]

Consensus sequences

A likely general USF box consensus sequence may be 3'-GCC(A/T)NN(C/G/T)(A/G)-5'.

Human genes

Gene ID: 7391 is USF1 upstream transcription factor 1 (aka upstream stimulatory factor 1). "This gene encodes a member of the basic helix-loop-helix leucine zipper family, and can function as a cellular transcription factor. The encoded protein can activate transcription through pyrimidine-rich initiator (Inr) elements and E-box motifs. This gene has been linked to familial combined hyperlipidemia (FCHL). Alternative splicing of this gene results in multiple transcript variants. A related pseudogene has been defined on chromosome 21."[4]

  1. NP_009053.1 upstream stimulatory factor 1 isoform 1 (variant 1).
  2. NP_996888.1 upstream stimulatory factor 1 isoform 2 (variant 2).
  3. NP_001263302.1 upstream stimulatory factor 1 isoform 1 (variant 3).

Gene ID: 7392 is USF2 upstream transcription factor 2, c-fos interacting. "This gene encodes a member of the basic helix-loop-helix leucine zipper family of transcription factors. The encoded protein can activate transcription through pyrimidine-rich initiator (Inr) elements and E-box motifs and is involved in regulating multiple cellular processes."[5]

  1. NP_003358.1 upstream stimulatory factor 2 isoform 1.
  2. NP_997174.1 upstream stimulatory factor 2 isoform 2.
  3. NP_001308079.1 upstream stimulatory factor 2 isoform 3.
  4. XP_024307452.1 upstream stimulatory factor 2 isoform X1.
  5. XP_005259254.1 upstream stimulatory factor 2 isoform X2.
  6. XP_024307453.1 upstream stimulatory factor 2 isoform X3.
  7. XP_016882688.1 upstream stimulatory factor 2 isoform X4.
  8. XP_011525562.1 upstream stimulatory factor 2 isoform X5.
  9. XP_011525563.1 upstream stimulatory factor 2 isoform X6.

Gene ID: 205717 is USF3 upstream transcription factor family member 3. "This gene encodes a large protein that contains a helix-loop-helix domain and a polyglutamine region. A deletion in the polyglutamine region was associated with risk for thyroid carcinoma."[6]

  1. NP_001009899.3 basic helix-loop-helix domain-containing protein USF3 (variant 1).
  2. NR_111981.1 RNA Sequence (non-coding, variant 2).
  3. XP_024309159.1 basic helix-loop-helix domain-containing protein USF3 isoform X1.
  4. XP_024309160.1 basic helix-loop-helix domain-containing protein USF3 isoform X2.
  5. XP_016861360.1 basic helix-loop-helix domain-containing protein USF3 isoform X1.
  6. XP_016861361.1 basic helix-loop-helix domain-containing protein USF3 isoform X2.
  7. XP_005247265.2 basic helix-loop-helix domain-containing protein USF3 isoform X2.

Gene ID: 100151645 is USF1P1 upstream transcription factor 1 pseudogene 1.

Hypotheses

  1. A1BG has no USF boxes in either promoter.

USF samplings

Using the two versions of the consensus sequence and "⌘F" to locate these sequences in the nucleotides for A1BG listed in A1BG gene transcriptions revealed two occurrences (GCCTGGGA) and (GCCTTCCG) on the ZNF497 side.

For the Basic programs testing consensus sequence GCC(A/T)NN(C/G/T)(A/G) (starting with SuccessablesUSFbox.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), the programs are, are looking for, and found:

  1. Negative strand, negative direction: 11, GCCTGACG at 4329, GCCACCGA at 2529, GCCTCCGA at 2359, GCCACCGA at 2202, GCCTAGGG at 1814, GCCACCGA at 1767, GCCACTCG at 870, GCCTAGTG at 705, GCCACCGA at 658, GCCTAGTG at 432, GCCACCGA at 385.
  2. Positive strand, negative direction: 13, GCCTGGGA at 4302, GCCAGACG at 4235, GCCAGGCA at 4104, GCCAGGTG at 3953, GCCTGTCA at 3202, GCCACCCA at 3135, GCCAGGCA at 2521, GCCAGGTG at 2079, GCCAAAGG at 1639, GCCTCCCG at 1508, GCCAGGCA at 950, GCCAGGCA at 650, GCCATATG at 41.
  3. Negative strand, positive direction: 27, GCCTCCTG at 4408, GCCTTCCG at 4243, GCCTCAGA at 4195, GCCTGGGA at 3760, GCCACATG at 3707, GCCTGTGG at 3436, GCCAATGG at 2910, GCCTCTGG at 2883, GCCAAAGG at 2828, GCCAGGGA at 2576, GCCTCCCA at 2532, GCCTCCCA at 2396, GCCACCCA at 1853, GCCTTGGG at 1800, GCCTTTCA at 1601, GCCACCGG at 1546, GCCTTCCG at 1434, GCCTTCCG at 1334, GCCACCGG at 1294, GCCTCATG at 1238, GCCACACG at 986, GCCTGCCG at 909, GCCACACG at 886, GCCTGCCG at 809, GCCTTCCG at 678, GCCAGCGG at 331, GCCTGGGA at 288.
  4. Positive strand, positive direction: 4, GCCAACGG at 3492, GCCTCGTG at 1207, GCCTGACG at 748, GCCACCCG at 404.
  5. inverse complement, negative strand, negative direction: 0.
  6. inverse complement, positive strand, negative direction: 29, TGGGAGGC at 4273, CAGGAGGC at 4142, TGGGAGGC at 3991, TGGTTGGC at 3947, TAAGAGGC at 3896, TGGGAGGC at 3716, CAGATGGC at 3629, TAAAAGGC at 3442, CATCAGGC at 3397, CAGGAGGC at 3221, TGGGAGGC at 3082, TAGATGGC at 2907, CAGGAGGC at 2693, TGGAAGGC at 2559, TGGCAGGC at 2390, CCGGAGGC at 2358, TGGGAGGC at 2223, TGGGAGGC at 2106, TGGGAGGC at 1964, TGGGAGGC at 1797, TAGGAGGC at 1311, CAGGAGGC at 1279, TGGGAGGC at 1020, CAGGAGGC at 988, CAGGAGGC at 854, TGGGAGGC at 688, TGGGAGGC at 552, TGCGAGGC at 451, TGGGAGGC at 415.
  7. inverse complement, negative strand, positive direction: 22, CCTGAGGC at 4189, CAGCAGGC at 3695, CGGGAGGC at 3675, CAACAGGC at 3637, CATCTGGC at 3406, CCTCTGGC at 2984, CCTCTGGC at 2884, TGCAAGGC at 2694, CACCTGGC at 2570, CACCTGGC at 2434, TCTTAGGC at 2367, TCTCAGGC at 2116, TCTCTGGC at 1993, CGGCAGGC at 1906, CGAGAGGC at 1568, CGAGAGGC at 1484, CGAGAGGC at 1384, TACCTGGC at 1200, CGTGTGGC at 1023, CAGGTGGC at 198, TCACAGGC at 158, CCTCAGGC at 91.
  8. inverse complement, positive strand, positive direction: 15, CGGAAGGC at 4243, CCGTTGGC at 3912, TCGGTGGC at 2562, CCAGAGGC at 1961, CAGGTGGC at 1845, TCGGTGGC at 1608, TCGGTGGC at 1545, CGGAAGGC at 1434, CGGAAGGC at 1334, TCGGTGGC at 1293, CGAAAGGC at 1098, CGGAAGGC at 678, CGTCTGGC at 441, TCCAAGGC at 307, TGGGTGGC at 74.

USF (4560-2846) UTRs

  1. Negative strand, negative direction: GCCTGACG at 4329.
  2. Positive strand, negative direction: GCCTGGGA at 4302, GCCAGACG at 4235, GCCAGGCA at 4104, GCCAGGTG at 3953, GCCTGTCA at 3202, GCCACCCA at 3135.
  3. Positive strand, negative direction: TGGGAGGC at 4273, CAGGAGGC at 4142, TGGGAGGC at 3991, TGGTTGGC at 3947, TAAGAGGC at 3896, TGGGAGGC at 3716, CAGATGGC at 3629, TAAAAGGC at 3442, CATCAGGC at 3397, CAGGAGGC at 3221, TGGGAGGC at 3082, TAGATGGC at 2907.

USF positive direction (4445-4265) core promoters

  1. Negative strand, positive direction: GCCTCCTG at 4408.

USF negative direction (2811-2596) proximal promoters

  1. Positive strand, negative direction: CAGGAGGC at 2693.

USF positive direction (4265-4050) proximal promoters

  1. Negative strand, positive direction: GCCTTCCG at 4243, GCCTCAGA at 4195.
  2. Negative strand, positive direction: CCTGAGGC at 4189.

USF negative direction (2596-1) distal promoters

  1. Negative strand, negative direction: GCCACCGA at 2529, GCCTCCGA at 2359, GCCACCGA at 2202, GCCTAGGG at 1814, GCCACCGA at 1767, GCCACTCG at 870, GCCTAGTG at 705, GCCACCGA at 658, GCCTAGTG at 432, GCCACCGA at 385.
  2. Positive strand, negative direction: GCCAGGCA at 2521, GCCAGGTG at 2079, GCCAAAGG at 1639, GCCTCCCG at 1508, GCCAGGCA at 950, GCCAGGCA at 650, GCCATATG at 41.
  3. Positive strand, negative direction: TGGAAGGC at 2559, TGGCAGGC at 2390, CCGGAGGC at 2358, TGGGAGGC at 2223, TGGGAGGC at 2106, TGGGAGGC at 1964, TGGGAGGC at 1797, TAGGAGGC at 1311, CAGGAGGC at 1279, TGGGAGGC at 1020, CAGGAGGC at 988, CAGGAGGC at 854, TGGGAGGC at 688, TGGGAGGC at 552, TGCGAGGC at 451, TGGGAGGC at 415.

USF positive direction (4050-1) distal promoters

  1. Negative strand, positive direction: GCCTGGGA at 3760, GCCACATG at 3707, GCCTGTGG at 3436, GCCAATGG at 2910, GCCTCTGG at 2883, GCCAAAGG at 2828, GCCAGGGA at 2576, GCCTCCCA at 2532, GCCTCCCA at 2396, GCCACCCA at 1853, GCCTTGGG at 1800, GCCTTTCA at 1601, GCCACCGG at 1546, GCCTTCCG at 1434, GCCTTCCG at 1334, GCCACCGG at 1294, GCCTCATG at 1238, GCCACACG at 986, GCCTGCCG at 909, GCCACACG at 886, GCCTGCCG at 809, GCCTTCCG at 678, GCCAGCGG at 331, GCCTGGGA at 288.
  2. Negative strand, positive direction: CAGCAGGC at 3695, CGGGAGGC at 3675, CAACAGGC at 3637, CATCTGGC at 3406, CCTCTGGC at 2984, CCTCTGGC at 2884, TGCAAGGC at 2694, CACCTGGC at 2570, CACCTGGC at 2434, TCTTAGGC at 2367, TCTCAGGC at 2116, TCTCTGGC at 1993, CGGCAGGC at 1906, CGAGAGGC at 1568, CGAGAGGC at 1484, CGAGAGGC at 1384, TACCTGGC at 1200, CGTGTGGC at 1023, CAGGTGGC at 198, TCACAGGC at 158, CCTCAGGC at 91.
  3. Positive strand, positive direction: GCCAACGG at 3492, GCCTCGTG at 1207, GCCTGACG at 748, GCCACCCG at 404.
  4. Positive strand, positive direction: CCGTTGGC at 3912, TCGGTGGC at 2562, CCAGAGGC at 1961, CAGGTGGC at 1845, TCGGTGGC at 1608, TCGGTGGC at 1545, CGGAAGGC at 1434, CGGAAGGC at 1334, TCGGTGGC at 1293, CGAAAGGC at 1098, CGGAAGGC at 678, CGTCTGGC at 441, TCCAAGGC at 307, TGGGTGGC at 74.

USF random dataset samplings

  1. RDr0: 0.
  2. RDr1: 0.
  3. RDr2: 0.
  4. RDr3: 0.
  5. RDr4: 0.
  6. RDr5: 0.
  7. RDr6: 0.
  8. RDr7: 0.
  9. RDr8: 0.
  10. RDr9: 0.
  11. RDr0ci: 0.
  12. RDr1ci: 0.
  13. RDr2ci: 0.
  14. RDr3ci: 0.
  15. RDr4ci: 0.
  16. RDr5ci: 0.
  17. RDr6ci: 0.
  18. RDr7ci: 0.
  19. RDr8ci: 0.
  20. RDr9ci: 0.

RDr arbitrary (evens) (4560-2846) UTRs

RDr alternate (odds) (4560-2846) UTRs

RDr arbitrary negative direction (evens) (2846-2811) core promoters

RDr alternate negative direction (odds) (2846-2811) core promoters

RDr arbitrary positive direction (odds) (4445-4265) core promoters

RDr alternate positive direction (evens) (4445-4265) core promoters

RDr arbitrary negative direction (evens) (2811-2596) proximal promoters

RDr alternate negative direction (odds) (2811-2596) proximal promoters

RDr arbitrary positive direction (odds) (4265-4050) proximal promoters

RDr alternate positive direction (evens) (4265-4050) proximal promoters

RDr arbitrary negative direction (evens) (2596-1) distal promoters

RDr alternate negative direction (odds) (2596-1) distal promoters

RDr arbitrary positive direction (odds) (4050-1) distal promoters

RDr alternate positive direction (evens) (4050-1) distal promoters

USF analysis and results

Main article: Complex locus A1BG and ZNF497 § USFs

"GCCATCTG, which contains a consensus sequence, CANNTG"[3], + "GCCACCGG."[3] which suggests GCCANN(G/T)G. Adding in a portion in the rat insulin 2 gene the equivalent sequence is GCCACCCA yields GCCANN(C/G/T)(A/G).[3]

Using the two versions of the consensus sequence and "⌘F" to locate these sequences in the nucleotides for A1BG listed in A1BG gene transcriptions revealed two occurrences (GCCTGGGA) and (GCCTTCCG) on the ZNF497 side. Combining these with GCCANN(C/G/T)(A/G)[3] suggests GCC(A/T)NN(C/G/T)(A/G).

Reals or randoms Promoters direction Numbers Strands Occurrences Averages (± 0.1)
Reals UTR negative 19,13 2 9.5,6.5 9.5 ± 8.5 (--1,+-18),6.5 ± 6.5 (--0,+-13)
Randoms UTR arbitrary negative 0 10 0 0
Randoms UTR alternate negative 0 10 0 0
Reals Core negative 0 2 0 0
Randoms Core arbitrary negative 0 10 0 0
Randoms Core alternate negative 0 10 0 0
Reals Core positive 1 2 0.5 0.5
Randoms Core arbitrary positive 0 10 0 0
Randoms Core alternate positive 0 10 0 0
Reals Proximal negative 1 2 0.5 0.5 ± 0.5 (+-1,--0)
Randoms Proximal arbitrary negative 0 10 0 0
Randoms Proximal alternate negative 0 10 0 0
Reals Proximal positive 3 2 1.5 1.5 ± 1.5 (-+3,++0)
Randoms Proximal arbitrary positive 0 10 0 0
Randoms Proximal alternate positive 0 10 0 0
Reals Distal negative 33 2 16.5 16.5 ± 6.5 (--10,+-23)
Randoms Distal arbitrary negative 0 10 0 0
Randoms Distal alternate negative 0 10 0 0
Reals Distal positive 63 2 31.5 31.5 ± 13.5 (-+45,++18)
Randoms Distal arbitrary positive 0 10 0 0
Randoms Distal alternate positive 0 10 0 0

Comparison:

The occurrences of real USFs are greater than the randoms. This suggests that the real USFs are likely active or activable.

See also

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Marie-Dominique Galibert, Suzanne Carreira, and Colin R. Goding (2001 September 3). "The Usf-1 transcription factor is a novel target for the stress-responsive p38 kinase and mediates UV-induced Tyrosinase expression". EMBO Journal. 20 (17): 5022–5031. doi:10.1093/emboj/20.17.5022. Retrieved 7 December 2018. Check date values in: |date= (help)
  2. ↑ 2.0 2.1 Libo Sa, Yan Li, Lini Zhao1, Yunhui Liu, Ping Wang, Libo Liu, Zhen Li, Jun Ma, Heng Cai and Yixue Xue (28 June 2017). "The Role of HOTAIR/miR-148b-3p/USF1 on Regulating the Permeability of BTB". Frontiers in Molecular Neuroscience. 10 (194): 194. doi:10.3389/fnmol.2017.00194. Retrieved 20 August 2020.
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 Martin L. Read, Andrew R. Clark and Kevin Docherty (1993). "The helix-loop-helix transcription factor USF (upstream stimulating factor) binds to a regulatory sequence of the human insulin gene enhancer" (PDF). Biochemical Journal. 295: 233–237. Retrieved 14 August 2020.
  4. ↑ RefSeq (February 2013). "USF1 upstream transcription factor 1 [ Homo sapiens (human) ]". 8600 Rockville Pike, Bethesda MD, 20894 USA: National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 10 December 2018.
  5. ↑ RefSeq (March 2016). "USF2 upstream transcription factor 2, c-fos interacting [ Homo sapiens (human) ]". 8600 Rockville Pike, Bethesda MD, 20894 USA: National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 10 December 2018.
  6. ↑ RefSeq (May 2017). "USF3 upstream transcription factor family member 3 [ Homo sapiens (human) ]". 8600 Rockville Pike, Bethesda MD, 20894 USA: National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 10 December 2018.

External links

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